@article{21708, abstract = {On October 4, 2023, a proglacial lake named the South Lhonak lake was the source of a catastrophic Glacier Lake Outburst Flood (GLOF) in the Teesta river basin area, resulting in 24 fatalities and leaving over 70 persons missing. The GLOF also destroyed 13 bridges and a major hydropower plant in the Chungthang region. Over 60,000 individuals in four districts of Sikkim were impacted by this GLOF event. This study examines the factors that led to the GLOF event. Our study shows that the cause of this GLOF was initiated by a landslide, that dumped a substantial amount (~ 38.31 million m3) of debris into the South Lhonak Lake. Furthermore, the glacier that was connected to the lake, lost a big chunk of ice mass (~ 7 million m3) due to calving. The combination of these two processes led to the collapse of the left lateral moraine that consequently generated flood waves which breached the terminal moraine dam of the lake. We recommend monitoring land subsidence and calving events for large proglacial lakes to prevent the disastrous consequences of such GLOFs in the future.}, author = {Mohanty, Litan Kumar and Gantayat, Prateek and Dixit, Ankur and Das Adhikari, Manik and Biswas, Rahul and Singh, Vivek Kumar}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{Sequence of events that led to the South Lhonak lake outburst flood in Sikkim, India}}, doi = {10.1038/s41598-026-35895-7}, volume = {16}, year = {2026}, } @article{19366, abstract = {Staphylococcus aureus (S. aureus) is one of the most common causative agents of mammary gland infection and mastitis, but the specific role of S. aureus-derived extracellular vesicles (SaEVs) in mastitis has been poorly studied to date. Here, we aimed to investigate the response of bovine monocyte-derived macrophages (boMdM) to SaEVs of the genotype B (GTB) mastitis-related strain M5512B. Specifically, we evaluated the effects on the actin cytoskeleton, gene expression, and the SaEV proteomic cargo. Furthermore, we assessed to what extent the cellular and molecular response of boMdM to SaEVs differed from peripheral mononuclear blood cells (PBMCs) used for in vitro derivation of the former. We observed that SaEVs induced morphological changes in boMdM, leading to a pro-inflammatory and pyroptosis-related increased gene expression. Additionally, our study revealed that boMdM and PBMCs exhibited stimulus-specific differing responses. The proteomic analysis of SaEVs identified clusters of proteins related to virulence and antibiotic resistance, supporting the theory that S. aureus might use EVs to evade host defences and colonize the mammary gland. Our results bring new insights into how SaEVs might impact the host during an S. aureus infection, which can be useful for future S. aureus vaccine development.}, author = {Saenz-De-Juano, Mara D. and Silvestrelli, Giulia and Buri, Samuel and Zinsli, Léa V. and Schmelcher, Mathias and Ulbrich, Susanne E.}, issn = {2045-2322}, journal = {Scientific Reports}, pages = {6059}, publisher = {Springer Nature}, title = {{Mastitis-related Staphylococcus aureus-derived extracellular vesicles induce a pro-inflammatory response in bovine monocyte-derived macrophages}}, doi = {10.1038/s41598-025-90466-6}, volume = {15}, year = {2025}, } @article{19529, abstract = {NRF2 is a transcription factor responsible for coordinating the expression of over a thousand cytoprotective genes. Although NRF2 is constitutively expressed, its stability is modulated by the redox-sensitive protein KEAP1 and other conditional binding partner regulators. The new era of NRF2 research has highlighted the cooperation between NRF2 and PIN1 in modifying its cytoprotective effect. Despite numerous studies, the understanding of the PIN1-NRF2 interaction remains limited. Herein, we described the binding interaction of PIN1 and three different 14-mer long phospho-peptides mimicking NRF2 protein using computer-based, biophysical, and biochemical approaches. According to our computational analyses, the residues positioned in the WW domain of PIN1 (Ser16, Arg17, Ser18, Tyr23, Ser32, Gln33, and Trp34) were found to be crucial for PIN1-NRF2 interactions. Biophysical FP assays were used to verify the computational prediction. The data demonstrated that Pintide, a peptide predominantly interacting with the PIN1 WW-domain, led to a significant reduction in the binding affinity of the NRF2 mimicking peptides. Moreover, we evaluated the impact of known PIN1 inhibitors (juglone, KPT-6566, and EGCG) on the PIN1-NRF2 interaction. Among the inhibitors, KPT-6566 showed the most potent inhibitory effect on PIN1-NRF2 interaction within an IC50 range of 0.3–1.4 µM. Furthermore, our mass spectrometry analyses showed that KPT-6566 appeared to covalently modify PIN1 via conjugate addition, rather than disulfide exchange of the sulfonyl-acetate moiety. Altogether, such inhibitors would also be highly valuable molecular probes for further investigation of PIN1 regulation of NRF2 in the cellular context and potentially pave the way for drug molecules that specifically inhibit the cytoprotective effects of NRF2 in cancer.}, author = {Ozleyen, Adem and Duran, Gizem Nur and Dönmez, Serhat and Ozbil, Mehmet and Doveston, Richard G. and Tumer, Tugba Boyunegmez}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{Identification and inhibition of PIN1-NRF2 protein–protein interactions through computational and biophysical approaches}}, doi = {10.1038/s41598-025-89342-0}, volume = {15}, year = {2025}, } @article{12329, abstract = {In this article, we develop two independent and new approaches to model epidemic spread in a network. Contrary to the most studied models, those developed here allow for contacts with different probabilities of transmitting the disease (transmissibilities). We then examine each of these models using some mean field type approximations. The first model looks at the late-stage effects of an epidemic outbreak and allows for the computation of the probability that a given vertex was infected. This computation is based on a mean field approximation and only depends on the number of contacts and their transmissibilities. This approach shares many similarities with percolation models in networks. The second model we develop is a dynamic model which we analyze using a mean field approximation which highly reduces the dimensionality of the system. In particular, the original system which individually analyses each vertex of the network is reduced to one with as many equations as different transmissibilities. Perhaps the greatest contribution of this article is the observation that, in both these models, the existence and size of an epidemic outbreak are linked to the properties of a matrix which we call the R-matrix. This is a generalization of the basic reproduction number which more precisely characterizes the main routes of infection.}, author = {Gómez, Arturo and Oliveira, Goncalo}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{New approaches to epidemic modeling on networks}}, doi = {10.1038/s41598-022-19827-9}, volume = {13}, year = {2023}, } @article{13166, abstract = {Brachyury, a member of T-box gene family, is widely known for its major role in mesoderm specification in bilaterians. It is also present in non-bilaterian metazoans, such as cnidarians, where it acts as a component of an axial patterning system. In this study, we present a phylogenetic analysis of Brachyury genes within phylum Cnidaria, investigate differential expression and address a functional framework of Brachyury paralogs in hydrozoan Dynamena pumila. Our analysis indicates two duplication events of Brachyury within the cnidarian lineage. The first duplication likely appeared in the medusozoan ancestor, resulting in two copies in medusozoans, while the second duplication arose in the hydrozoan ancestor, resulting in three copies in hydrozoans. Brachyury1 and 2 display a conservative expression pattern marking the oral pole of the body axis in D. pumila. On the contrary, Brachyury3 expression was detected in scattered presumably nerve cells of the D. pumila larva. Pharmacological modulations indicated that Brachyury3 is not under regulation of cWnt signaling in contrast to the other two Brachyury genes. Divergence in expression patterns and regulation suggest neofunctionalization of Brachyury3 in hydrozoans.}, author = {Vetrova, Alexandra A. and Kupaeva, Daria M. and Kizenko, Alena and Lebedeva, Tatiana S. and Walentek, Peter and Tsikolia, Nikoloz and Kremnyov, Stanislav V.}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{The evolutionary history of Brachyury genes in Hydrozoa involves duplications, divergence, and neofunctionalization}}, doi = {10.1038/s41598-023-35979-8}, volume = {13}, year = {2023}, } @article{10731, abstract = {Motivated by COVID-19, we develop and analyze a simple stochastic model for the spread of disease in human population. We track how the number of infected and critically ill people develops over time in order to estimate the demand that is imposed on the hospital system. To keep this demand under control, we consider a class of simple policies for slowing down and reopening society and we compare their efficiency in mitigating the spread of the virus from several different points of view. We find that in order to avoid overwhelming of the hospital system, a policy must impose a harsh lockdown or it must react swiftly (or both). While reacting swiftly is universally beneficial, being harsh pays off only when the country is patient about reopening and when the neighboring countries coordinate their mitigation efforts. Our work highlights the importance of acting decisively when closing down and the importance of patience and coordination between neighboring countries when reopening.}, author = {Svoboda, Jakub and Tkadlec, Josef and Pavlogiannis, Andreas and Chatterjee, Krishnendu and Nowak, Martin A.}, issn = {2045-2322}, journal = {Scientific Reports}, number = {1}, publisher = {Springer Nature}, title = {{Infection dynamics of COVID-19 virus under lockdown and reopening}}, doi = {10.1038/s41598-022-05333-5}, volume = {12}, year = {2022}, } @article{10069, abstract = {The extent to which women differ in the course of blood cell counts throughout pregnancy, and the importance of these changes to pregnancy outcomes has not been well defined. Here, we develop a series of statistical analyses of repeated measures data to reveal the degree to which women differ in the course of pregnancy, predict the changes that occur, and determine the importance of these changes for post-partum hemorrhage (PPH) which is one of the leading causes of maternal mortality. We present a prospective cohort of 4082 births recorded at the University Hospital, Lausanne, Switzerland between 2009 and 2014 where full labour records could be obtained, along with complete blood count data taken at hospital admission. We find significant differences, at a [Formula: see text] level, among women in how blood count values change through pregnancy for mean corpuscular hemoglobin, mean corpuscular volume, mean platelet volume, platelet count and red cell distribution width. We find evidence that almost all complete blood count values show trimester-specific associations with PPH. For example, high platelet count (OR 1.20, 95% CI 1.01-1.53), high mean platelet volume (OR 1.58, 95% CI 1.04-2.08), and high erythrocyte levels (OR 1.36, 95% CI 1.01-1.57) in trimester 1 increased PPH, but high values in trimester 3 decreased PPH risk (OR 0.85, 0.79, 0.67 respectively). We show that differences among women in the course of blood cell counts throughout pregnancy have an important role in shaping pregnancy outcome and tracking blood count value changes through pregnancy improves identification of women at increased risk of postpartum hemorrhage. This study provides greater understanding of the complex changes in blood count values that occur through pregnancy and provides indicators to guide the stratification of patients into risk groups.}, author = {Robinson, Matthew Richard and Patxot, Marion and Stojanov, Miloš and Blum, Sabine and Baud, David}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{Postpartum hemorrhage risk is driven by changes in blood composition through pregnancy}}, doi = {10.1038/s41598-021-98411-z}, volume = {11}, year = {2021}, } @article{9097, abstract = {Psoriasis is a chronic inflammatory skin disease clinically characterized by the appearance of red colored, well-demarcated plaques with thickened skin and with silvery scales. Recent studies have established the involvement of a complex signalling network of interactions between cytokines, immune cells and skin cells called keratinocytes. Keratinocytes form the cells of the outermost layer of the skin (epidermis). Visible plaques in psoriasis are developed due to the fast proliferation and unusual differentiation of keratinocyte cells. Despite that, the exact mechanism of the appearance of these plaques in the cytokine-immune cell network is not clear. A mathematical model embodying interactions between key immune cells believed to be involved in psoriasis, keratinocytes and relevant cytokines has been developed. The complex network formed of these interactions poses several challenges. Here, we choose to study subnetworks of this complex network and initially focus on interactions involving TNFα, IL-23/IL-17, and IL-15. These are chosen based on known evidence of their therapeutic efficacy. In addition, we explore the role of IL-15 in the pathogenesis of psoriasis and its potential as a future drug target for a novel treatment option. We perform steady state analyses for these subnetworks and demonstrate that the interactions between cells, driven by cytokines could cause the emergence of a psoriasis state (hyper-proliferation of keratinocytes) when levels of TNFα, IL-23/IL-17 or IL-15 are increased. The model results explain and support the clinical potentiality of anti-cytokine treatments. Interestingly, our results suggest different dynamic scenarios underpin the pathogenesis of psoriasis, depending upon the dominant cytokines of subnetworks. We observed that the increase in the level of IL-23/IL-17 and IL-15 could lead to psoriasis via a bistable route, whereas an increase in the level of TNFα would lead to a monotonic and gradual disease progression. Further, we demonstrate how this insight, bistability, could be exploited to improve the current therapies and develop novel treatment strategies for psoriasis.}, author = {Pandey, Rakesh and Al-Nuaimi, Yusur and Mishra, Rajiv Kumar and Spurgeon, Sarah K. and Goodfellow, Marc}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{Role of subnetworks mediated by TNF α, IL-23/IL-17 and IL-15 in a network involved in the pathogenesis of psoriasis}}, doi = {10.1038/s41598-020-80507-7}, volume = {11}, year = {2021}, } @article{9905, abstract = {Vaccines are thought to be the best available solution for controlling the ongoing SARS-CoV-2 pandemic. However, the emergence of vaccine-resistant strains may come too rapidly for current vaccine developments to alleviate the health, economic and social consequences of the pandemic. To quantify and characterize the risk of such a scenario, we created a SIR-derived model with initial stochastic dynamics of the vaccine-resistant strain to study the probability of its emergence and establishment. Using parameters realistically resembling SARS-CoV-2 transmission, we model a wave-like pattern of the pandemic and consider the impact of the rate of vaccination and the strength of non-pharmaceutical intervention measures on the probability of emergence of a resistant strain. As expected, we found that a fast rate of vaccination decreases the probability of emergence of a resistant strain. Counterintuitively, when a relaxation of non-pharmaceutical interventions happened at a time when most individuals of the population have already been vaccinated the probability of emergence of a resistant strain was greatly increased. Consequently, we show that a period of transmission reduction close to the end of the vaccination campaign can substantially reduce the probability of resistant strain establishment. Our results suggest that policymakers and individuals should consider maintaining non-pharmaceutical interventions and transmission-reducing behaviours throughout the entire vaccination period.}, author = {Rella, Simon and Kulikova, Yuliya A. and Dermitzakis, Emmanouil T. and Kondrashov, Fyodor}, issn = {2045-2322}, journal = {Scientific Reports}, number = {1}, publisher = {Springer Nature}, title = {{Rates of SARS-CoV-2 transmission and vaccination impact the fate of vaccine-resistant strains}}, doi = {10.1038/s41598-021-95025-3}, volume = {11}, year = {2021}, } @article{9997, abstract = {Indirect reciprocity is a mechanism for the evolution of cooperation based on social norms. This mechanism requires that individuals in a population observe and judge each other’s behaviors. Individuals with a good reputation are more likely to receive help from others. Previous work suggests that indirect reciprocity is only effective when all relevant information is reliable and publicly available. Otherwise, individuals may disagree on how to assess others, even if they all apply the same social norm. Such disagreements can lead to a breakdown of cooperation. Here we explore whether the predominantly studied ‘leading eight’ social norms of indirect reciprocity can be made more robust by equipping them with an element of generosity. To this end, we distinguish between two kinds of generosity. According to assessment generosity, individuals occasionally assign a good reputation to group members who would usually be regarded as bad. According to action generosity, individuals occasionally cooperate with group members with whom they would usually defect. Using individual-based simulations, we show that the two kinds of generosity have a very different effect on the resulting reputation dynamics. Assessment generosity tends to add to the overall noise and allows defectors to invade. In contrast, a limited amount of action generosity can be beneficial in a few cases. However, even when action generosity is beneficial, the respective simulations do not result in full cooperation. Our results suggest that while generosity can favor cooperation when individuals use the most simple strategies of reciprocity, it is disadvantageous when individuals use more complex social norms.}, author = {Schmid, Laura and Shati, Pouya and Hilbe, Christian and Chatterjee, Krishnendu}, issn = {2045-2322}, journal = {Scientific Reports}, keywords = {Multidisciplinary}, number = {1}, publisher = {Springer Nature}, title = {{The evolution of indirect reciprocity under action and assessment generosity}}, doi = {10.1038/s41598-021-96932-1}, volume = {11}, year = {2021}, } @article{7632, abstract = {The posterior parietal cortex (PPC) and frontal motor areas comprise a cortical network supporting goal-directed behaviour, with functions including sensorimotor transformations and decision making. In primates, this network links performed and observed actions via mirror neurons, which fire both when individuals perform an action and when they observe the same action performed by a conspecific. Mirror neurons are believed to be important for social learning, but it is not known whether mirror-like neurons occur in similar networks in other social species, such as rodents, or if they can be measured in such models using paradigms where observers passively view a demonstrator. Therefore, we imaged Ca2+ responses in PPC and secondary motor cortex (M2) while mice performed and observed pellet-reaching and wheel-running tasks, and found that cell populations in both areas robustly encoded several naturalistic behaviours. However, neural responses to the same set of observed actions were absent, although we verified that observer mice were attentive to performers and that PPC neurons responded reliably to visual cues. Statistical modelling also indicated that executed actions outperformed observed actions in predicting neural responses. These results raise the possibility that sensorimotor action recognition in rodents could take place outside of the parieto-frontal circuit, and underscore that detecting socially-driven neural coding depends critically on the species and behavioural paradigm used.}, author = {Tombaz, Tuce and Dunn, Benjamin A. and Hovde, Karoline and Cubero, Ryan J and Mimica, Bartul and Mamidanna, Pranav and Roudi, Yasser and Whitlock, Jonathan R.}, issn = {2045-2322}, journal = {Scientific reports}, number = {1}, publisher = {Springer Nature}, title = {{Action representation in the mouse parieto-frontal network}}, doi = {10.1038/s41598-020-62089-6}, volume = {10}, year = {2020}, } @article{7931, abstract = {In the course of sample preparation for Next Generation Sequencing (NGS), DNA is fragmented by various methods. Fragmentation shows a persistent bias with regard to the cleavage rates of various dinucleotides. With the exception of CpG dinucleotides the previously described biases were consistent with results of the DNA cleavage in solution. Here we computed cleavage rates of all dinucleotides including the methylated CpG and unmethylated CpG dinucleotides using data of the Whole Genome Sequencing datasets of the 1000 Genomes project. We found that the cleavage rate of CpG is significantly higher for the methylated CpG dinucleotides. Using this information, we developed a classifier for distinguishing cancer and healthy tissues based on their CpG islands statuses of the fragmentation. A simple Support Vector Machine classifier based on this algorithm shows an accuracy of 84%. The proposed method allows the detection of epigenetic markers purely based on mechanochemical DNA fragmentation, which can be detected by a simple analysis of the NGS sequencing data.}, author = {Uroshlev, Leonid A. and Abdullaev, Eldar T. and Umarova, Iren R. and Il’Icheva, Irina A. and Panchenko, Larisa A. and Polozov, Robert V. and Kondrashov, Fyodor and Nechipurenko, Yury D. and Grokhovsky, Sergei L.}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{A method for identification of the methylation level of CpG islands from NGS data}}, doi = {10.1038/s41598-020-65406-1}, volume = {10}, year = {2020}, } @article{8643, abstract = {The parabigeminal nucleus (PBG) is the mammalian homologue to the isthmic complex of other vertebrates. Optogenetic stimulation of the PBG induces freezing and escape in mice, a result thought to be caused by a PBG projection to the central nucleus of the amygdala. However, the isthmic complex, including the PBG, has been classically considered satellite nuclei of the Superior Colliculus (SC), which upon stimulation of its medial part also triggers fear and avoidance reactions. As the PBG-SC connectivity is not well characterized, we investigated whether the topology of the PBG projection to the SC could be related to the behavioral consequences of PBG stimulation. To that end, we performed immunohistochemistry, in situ hybridization and neural tracer injections in the SC and PBG in a diurnal rodent, the Octodon degus. We found that all PBG neurons expressed both glutamatergic and cholinergic markers and were distributed in clearly defined anterior (aPBG) and posterior (pPBG) subdivisions. The pPBG is connected reciprocally and topographically to the ipsilateral SC, whereas the aPBG receives afferent axons from the ipsilateral SC and projected exclusively to the contralateral SC. This contralateral projection forms a dense field of terminals that is restricted to the medial SC, in correspondence with the SC representation of the aerial binocular field which, we also found, in O. degus prompted escape reactions upon looming stimulation. Therefore, this specialized topography allows binocular interactions in the SC region controlling responses to aerial predators, suggesting a link between the mechanisms by which the SC and PBG produce defensive behaviors.}, author = {Deichler, Alfonso and Carrasco, Denisse and Lopez-Jury, Luciana and Vega Zuniga, Tomas A and Marquez, Natalia and Mpodozis, Jorge and Marin, Gonzalo}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{A specialized reciprocal connectivity suggests a link between the mechanisms by which the superior colliculus and parabigeminal nucleus produce defensive behaviors in rodents}}, doi = {10.1038/s41598-020-72848-0}, volume = {10}, year = {2020}, } @article{7487, abstract = {Glutaminase (GA) catalyzes the first step in mitochondrial glutaminolysis playing a key role in cancer metabolic reprogramming. Humans express two types of GA isoforms: GLS and GLS2. GLS isozymes have been consistently related to cell proliferation, but the role of GLS2 in cancer remains poorly understood. GLS2 is repressed in many tumor cells and a better understanding of its function in tumorigenesis may further the development of new therapeutic approaches. We analyzed GLS2 expression in HCC, GBM and neuroblastoma cells, as well as in monkey COS-7 cells. We studied GLS2 expression after induction of differentiation with phorbol ester (PMA) and transduction with the full-length cDNA of GLS2. In parallel, we investigated cell cycle progression and levels of p53, p21 and c-Myc proteins. Using the baculovirus system, human GLS2 protein was overexpressed, purified and analyzed for posttranslational modifications employing a proteomics LC-MS/MS platform. We have demonstrated a dual targeting of GLS2 in human cancer cells. Immunocytochemistry and subcellular fractionation gave consistent results demonstrating nuclear and mitochondrial locations, with the latter being predominant. Nuclear targeting was confirmed in cancer cells overexpressing c-Myc- and GFP-tagged GLS2 proteins. We assessed the subnuclear location finding a widespread distribution of GLS2 in the nucleoplasm without clear overlapping with specific nuclear substructures. GLS2 expression and nuclear accrual notably increased by treatment of SH-SY5Y cells with PMA and it correlated with cell cycle arrest at G2/M, upregulation of tumor suppressor p53 and p21 protein. A similar response was obtained by overexpression of GLS2 in T98G glioma cells, including downregulation of oncogene c-Myc. Furthermore, human GLS2 was identified as being hypusinated by MS analysis, a posttranslational modification which may be relevant for its nuclear targeting and/or function. Our studies provide evidence for a tumor suppressor role of GLS2 in certain types of cancer. The data imply that GLS2 can be regarded as a highly mobile and multilocalizing protein translocated to both mitochondria and nuclei. Upregulation of GLS2 in cancer cells induced an antiproliferative response with cell cycle arrest at the G2/M phase.}, author = {López De La Oliva, Amada R. and Campos-Sandoval, José A. and Gómez-García, María C. and Cardona, Carolina and Martín-Rufián, Mercedes and Sialana, Fernando J. and Castilla, Laura and Bae, Narkhyun and Lobo, Carolina and Peñalver, Ana and García-Frutos, Marina and Carro, David and Enrique, Victoria and Paz, José C. and Mirmira, Raghavendra G. and Gutiérrez, Antonia and Alonso, Francisco J. and Segura, Juan A. and Matés, José M. and Lubec, Gert and Márquez, Javier}, issn = {2045-2322}, journal = {Scientific reports}, number = {1}, publisher = {Springer Nature}, title = {{Nuclear translocation of glutaminase GLS2 in human cancer cells associates with proliferation arrest and differentiation}}, doi = {10.1038/s41598-020-58264-4}, volume = {10}, year = {2020}, } @article{6867, abstract = {A novel magnetic scratch method achieves repeatability, reproducibility and geometric control greater than pipette scratch assays and closely approximating the precision of cell exclusion assays while inducing the cell injury inherently necessary for wound healing assays. The magnetic scratch is affordable, easily implemented and standardisable and thus may contribute toward better comparability of data generated in different studies and laboratories.}, author = {Fenu, M. and Bettermann, T. and Vogl, C. and Darwish-Miranda, Nasser and Schramel, J. and Jenner, F. and Ribitsch, I.}, issn = {2045-2322}, journal = {Scientific Reports}, number = {1}, publisher = {Springer Nature}, title = {{A novel magnet-based scratch method for standardisation of wound-healing assays}}, doi = {10.1038/s41598-019-48930-7}, volume = {9}, year = {2019}, } @article{7095, abstract = {BAX, a member of the BCL2 gene family, controls the committed step of the intrinsic apoptotic program. Mitochondrial fragmentation is a commonly observed feature of apoptosis, which occurs through the process of mitochondrial fission. BAX has consistently been associated with mitochondrial fission, yet how BAX participates in the process of mitochondrial fragmentation during apoptosis remains to be tested. Time-lapse imaging of BAX recruitment and mitochondrial fragmentation demonstrates that rapid mitochondrial fragmentation during apoptosis occurs after the complete recruitment of BAX to the mitochondrial outer membrane (MOM). The requirement of a fully functioning BAX protein for the fission process was demonstrated further in BAX/BAK-deficient HCT116 cells expressing a P168A mutant of BAX. The mutant performed fusion to restore the mitochondrial network. but was not demonstrably recruited to the MOM after apoptosis induction. Under these conditions, mitochondrial fragmentation was blocked. Additionally, we show that loss of the fission protein, dynamin-like protein 1 (DRP1), does not temporally affect the initiation time or rate of BAX recruitment, but does reduce the final level of BAX recruited to the MOM during the late phase of BAX recruitment. These correlative observations suggest a model where late-stage BAX oligomers play a functional part of the mitochondrial fragmentation machinery in apoptotic cells.}, author = {Maes, Margaret E and Grosser, J. A. and Fehrman, R. L. and Schlamp, C. L. and Nickells, R. W.}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Springer Nature}, title = {{Completion of BAX recruitment correlates with mitochondrial fission during apoptosis}}, doi = {10.1038/s41598-019-53049-w}, volume = {9}, year = {2019}, } @article{390, abstract = {In the underdoped copper-oxides, high-temperature superconductivity condenses from a nonconventional metallic ”pseudogap” phase that exhibits a variety of non-Fermi liquid properties. Recently, it has become clear that a charge density wave (CDW) phase exists within the pseudogap regime. This CDW coexists and competes with superconductivity (SC) below the transition temperature Tc, suggesting that these two orders are intimately related. Here we show that the condensation of the superfluid from this unconventional precursor is reflected in deviations from the predictions of BSC theory regarding the recombination rate of quasiparticles. We report a detailed investigation of the quasiparticle (QP) recombination lifetime, τqp, as a function of temperature and magnetic field in underdoped HgBa2CuO4+δ (Hg-1201) and YBa2Cu3O6+x (YBCO) single crystals by ultrafast time-resolved reflectivity. We find that τqp(T) exhibits a local maximum in a small temperature window near Tc that is prominent in underdoped samples with coexisting charge order and vanishes with application of a small magnetic field. We explain this unusual, non-BCS behavior by positing that Tc marks a transition from phase-fluctuating SC/CDW composite order above to a SC/CDW condensate below. Our results suggest that the superfluid in underdoped cuprates is a condensate of coherently-mixed particle-particle and particle-hole pairs.}, author = {Hinton, James and Thewalt, E and Alpichshev, Zhanybek and Mahmood, Fahad and Koralek, Jake and Chan, Mun and Veit, Michael and Dorow, Chelsey and Barišić, Neven and Kemper, Alexander and Bonn, Doug and Hardy, Walter and Liang, Ruixing and Gedik, Nuh and Greven, Martin and Lanzara, Alessandra and Orenstein, Joseph}, issn = {2045-2322}, journal = {Scientific Reports}, publisher = {Nature Publishing Group}, title = {{The rate of quasiparticle recombination probes the onset of coherence in cuprate superconductors}}, doi = {10.1038/srep23610}, volume = {6}, year = {2016}, }