bluuebunny/crossref_metadata_2025_split huggingface dataset:
Global scientific research in Microbial Induced Calcite Precipitation: A bibliometric network analysis
Authors: Jarwar Mazhar Ali , Dumontet Stefano , Nastro Rosa Anna , Sanz-Montero M. Esther , Pasquale Vincenzo 
Published: October 2022

AbstractMicrobial Induced Calcite Precipitation (MICP) offers a host of interesting features, both from theoretical and practical standpoints. This process was firstly investigated as a geo-biological mechanism involved in carbonate mineral formation both in rocks and soil. The interest towards its practical use significantly increased in the recent years, as MICP was used in different fields, such as oil recovery, improvement of soil geotechnical characteristics and concreate healing. To the best of our knowledge, this paper is the first attempt to carry out a bibliometric descriptive study of publications on MICP. We analyzed data from the Web of Science Core Collection (WoSCC), which provides comprehensive information for bibliometric analysis, including the Science Citation Index-Expanded (SCI-E) and the Social Sciences Citation Index (SSCI). The bibliometric analysis was carried out on 1580 publications, from 2000 to August 2022, and included publication output, author, institution, country, collaborations between authors, institutes and countries, and citation frequency. We created visualization maps including research collaborations by using the VOSviewer program. MICP, carbonate precipitation, cementation, and soil improvement in terms of geotechnical properties are high-frequency used keywords. Although in the year 2000 only two papers were published on MICP, the number of publications increased rapidly since 2014. In 2021, 333 papers were published. China leads as the most productive country, followed by USA and Australia. According to our results, the number of research papers dramatically increased in the last 5 years. MICP with concrete healing/cementation, soil geotechnical improvement, and the low environmental impact of such a technique are becoming very popular topics among researchers. With the ageing of concrete buildings, as well as with the worsening of environmental pollution and soil alterations, the research about MICP will play an ever increasing and crucial role in civil engineering and geotechnical issues and in soil science. Nevertheless, our study pointed out a sort of concentration of the MICP studies in few countries. Russia and Brazil, for instance, seems to poorly contribute to MICP researches. A larger cooperation among countries, together with the extension of the research network on this topic, would considerably foster the progress in MICP studies, from both practical and speculative standpoints.
Dicentric chromosome breakage inDrosophila melanogasteris influenced by pericentric heterochromatin and reveals a novel class of fragile site
Authors: Hill Hunter , Bonser Danielle , Golic Kent G. 
Published: October 2022

ABSTRACTChromosome breakage plays an important role in the evolution of karyotypes, and can produce deleterious effects within a single individual, such as aneuploidy or cancer. Forces that influence how and where chromosomes break are not well understood. In humans, breakage tends to occur in conserved hotspots called common fragile sites (CFS), especially during replication stress. By following the fate of dicentric chromosomes inDrosophila melanogasterwe find that breakage under tension also tends to occur in specific hotspots. Our experimental approach was to induce sister chromatid exchange in a ring chromosome to generate a dicentric chromosome with a double chromatid bridge. In the following cell division, the dicentric bridges may break. We analyzed the breakage patterns of three different ring-Xchromosomes. These chromosomes differ by the amount and quality of heterochromatin they carry as well as their genealogical history. For all three chromosomes, breakage occurs preferentially in several hotspots. Surprisingly, we found that the hotspot locations are not conserved between the three chromosomes: each displays a unique array of breakage hotspots. The lack of hotspot conservation, along with a lack of response to aphidicolin, suggests that these breakage sites are not entirely analogous to CFS and may reveal new mechanisms of chromosome fragility.. Additionally, the frequency of dicentric breakage and the durability of their spindle attachment varies significantly between the three chromosomes and is correlated with the origin of the centromere and the amount of pericentric heterochromatin they carry. We suggest that different centromere strengths could account for this.
Chromosome-level genome assembly ofEuphorbia peplus, a model system for plant latex, reveals that relative lack of Ty3 transposons contributed to its small genome size
Authors: Johnson Arielle R. , Yue Yuanzheng , Carey Sarah B. , Park Se Jin , Kruse Lars H. , Bao Ashley , Harkess Alex , Pasha Asher , Provart Nicholas J. , Moghe Gaurav D. , Frank Margaret H. 
Published: October 2022

AbstractEuphorbia peplus(petty spurge) is a small, fast-growing plant that is native to Eurasia and has become a naturalized weed in North America and Australia.E. peplusis not only medicinally valuable, serving as a source for the skin cancer drug ingenol mebutate, but also has great potential as a model for latex production owing to its small size, ease of manipulation in the laboratory, and rapid reproductive cycle. To help establishE. peplusas a new model, we generated a 267.2 Mb HiC-anchored PacBio HiFi nuclear genome assembly with an embryophyta BUSCO score of 98.5%, a genome annotation based on RNA-seq data from six tissues, and publicly accessible tools including a genome browser and an interactive organ-specific expression atlas. Chromosome number is highly variable acrossEuphorbiaspecies. Using a comparative analysis of our newly sequencedE. peplusgenome with other Euphorbiaceae genomes, we show that variation inEuphorbiachromosome number is likely due to fragmentation and rearrangement rather than aneuploidy. Moreover, we found that theE. peplusgenome is relatively compact compared to related members of the genus in part due to restricted expansion of the Ty3 transposon family. Finally, we identify a large gene cluster that contains many previously identified enzymes in the putative ingenol mebutate biosynthesis pathway, along with additional gene candidates for this biosynthetic pathway. The genomic resources we have created forE. pepluswill help advance research on latex production and ingenol mebutate biosynthesis in the commercially important Euphorbiaceae family.Significance statementEuphorbiais one of the five largest genera in the plant kingdom. Despite an impressive phenotypic and metabolic diversity in this genus, only oneEuphorbiagenome has been sequenced so far, restricting insights intoEuphorbiabiology.Euphorbia peplushas excellent potential as a model species due to its latex production, fast growth rate and production of the anticancer drug ingenol mebutate. Here, we present a chromosome-levelE. peplusgenome assembly and publicly accessible resources to support molecular research for this unique species and the broader genus. We also provide an explanation of one reason the genome is so small, and identify more candidate genes for the anticancer drug and related compounds.
The possibility of anesthesia stimulated by a train of current pulses
Authors: Shneider Mikhail N. , Pekker Mikhail 
Published: October 2022

AbstractThis paper considers a simple theoretical model of blocking the passage of signals (action potentials) from sensory neurons and thereby effecting anesthesia without the use of anesthetics as a result of a sequence of unipolar current pulses generated by an external source. The proposed model allows the selection of parameters and the required frequency of the repetition of current pulses for the possible implementation of anesthesia depending on the electrical characteristics of the skin and the conductivity of the saline solution in which the myelinated nerve fibers are located.
A fast and versatile method for simultaneous HCR, immunohistochemistry and EdU labeling (SHInE)
Authors: Ćorić Aida , Stockinger Alexander W. , Schaffer Petra , Rokvić Dunja , Tessmar-Raible Kristin , Raible Florian 
Published: October 2022

AbstractAccess to newer, fast and cheap sequencing techniques, particularly on the single-cell level, have made transcriptomic data of tissues or single cells accessible to many researchers. As a consequence, there is increased need forin situvisualization of gene expression or encoded proteins to validate, localize or help interpret such sequencing data, as well as put them in context with cellular proliferation. A particular challenge for labeling and imaging transcripts are complex tissues that are often opaque and/or pigmented, preventing easy visual inspection. Here we introduce a versatile protocol that combinesin situhybridization chain reaction (HCR), immunohistochemistry (IHC) and proliferative cell labeling using 5-ethynyl-2’-deoxyuridine (EdU), and demonstrate its compatibility with tissue clearing. As a proof-of-concept, we show that our protocol allows for the parallel analysis of cell proliferation, gene expression and protein localization in bristleworm heads and trunks.
Distinct steady-state properties and TNF responses of epithelial long myosin light chain kinase (MLCK) splice variants
Authors: Chanez-Paredes Sandra D. , Abtahi Shabnam , Zha Juanmin , Zuo Li , He Weiqi , Turner Jerrold R. 
Published: October 2022

ABSTRACTIntestinal epithelia express two long myosin light chain kinase (MLCK) splice variants, MLCK1 and MLCK2. Unlike MLCK2, MLCK1 is concentrated at the perijunctional actomyosin ring and this localization is enhanced by tumor necrosis factor (TNF) signaling. Here we sought to identify and characterize the domain(s) that direct basal and TNF-induced MLCK1 subcellular localization. Quantitative morphometry demonstrated specific increases in MLCK1 expression and perijunctional localization in Crohn’s disease patient biopsies, relative to controls. TNF induced perijunctional recruitment of MLCK1-EGFP but did not affect localization of MLCK2-EGFP, which was predominantly associated with basal stress fibers. Recombinant N-terminal MLCK1 and MLCK2 regions accelerated actin polymerization in vitro but were not different from one another. In contrast, the affinity of N-terminal MLCK1 binding to F-actin was greater than that of MLCK2. Perijunctional MLCK1 and MLCK2 domain recruitment in intestinal epithelial cells paralleled in vitro F-actin binding. The unique MLCK1 Ig3 domain was necessary, but not sufficient, for both F-actin binding and perijunctional recruitment, but, nevertheless, displaced perijunctional MLCK1, enhanced steady-state barrier function, and limited TNF-induced MLCK1 recruitment and barrier loss. These data demonstrate selective perijunctional MLCK1 recruitment in Crohn’s disease, suggest that F-actin binding contributes to perijunctional recruitment, and show that Ig3 can act as a dominant negative effector that limits TNF-induced MLCK1 recruitment and barrier loss. These results data provide key mechanistic detail that will enable development of therapeutics that target Ig3, or its intercellular binding partners, to reverse inflammation-induced barrier loss and limit disease progression.
Declining autozygosity over time: an exploration in over 1 million individuals from three diverse cohorts
Authors: Colbert Sarah M.C. , Wendt Frank R. , Pathak Gita A. , Helmer Drew A. , Hauser Elizabeth R. , Keller Matthew C. , Polimanti Renato , Johnson Emma C. 
Published: October 2022

ABSTRACTWe hypothesized that overall autozygosity is decreasing over generational time. In this report, we present data that partially support this hypothesis from three large cohorts of diverse ancestries, two from the US (All of Us and the Million Veteran Program, N=82,474 and 622,497, respectively) and one from the UK (UK Biobank, N=380,899). Our results from a mixed-effect meta-analysis demonstrate an overall trend of decreasing autozygosity over generational time (meta-analyzed slope=-0.029, se=0.009, p=6.03e-4). Using a chi-square difference test, we determined that a model including an ancestry-by-country interaction term fit the data best, indicating that ancestry differences in this trend differ by country. We found further evidence to suggest a difference between the US and UK cohorts by meta-analyzing within country, observing a significant negative estimate in the US cohorts (meta-analyzed slope=-0.058, se=0.015, p=1.50e-4) but a non-significant estimate in the UK (meta-analyzed slope=-0.001, se=0.008, p=0.945). We also found that the association between autozygosity and year of birth in the overall meta-analysis was substantially attenuated when accounting for educational attainment and income (meta-analyzed slope=-0.011, se=0.008, p=0.167), suggesting that increases in education and income may partially account for decreasing levels of autozygosity over time. To our knowledge, this is the largest demonstration of decreasing autozygosity over time in a modern sample (birth years 1904-2003), and we speculate that this trend can be attributed to increases in population size, urbanization and panmixia, with differences in demographic and sociocultural processes leading to country-specific differences in the rate of decline.
JADE1 and HBO1/KAT7 proteins in the cytokinesis of epithelial cells. The role of PHD zinc fingers
Authors: Shao Bo , Panchenko Maria V. 
Published: October 2022

AbstractMembers of the conserved subfamily, JADE1S and JADE1L isoforms, are expressed in epithelial cells, fibroblasts, and epithelial cell lining in vivo. JADE1 proteins interact with histone acetyl transferase HBO1 complex. The two consecutive PHD zinc fingers of JADE1 bind chromatin. We recently reported novel effects of JADE1S on cytokinesis progression. JADE1S depletion facilitated G2/M-to-G1 transition and increased polyploidy and aneuploidy. JADE1S over-expression arrested cells in late cytokinesis, an effect reversed by AURKB inhibitor. In late cytokinesis cells JADE1S protein localized to the midbody. Results suggested a JADE1S role in final abscission delay. Here we investigated the expression of JADE1 in the central spindle, interactions with HBO1, and the role of PHD fingers in late cytokinesis arrest.The midzone begins to assemble in anaphase and forms into a midbody in cytokinesis. The midbody structure connects two daughter cells and is thought to bear factors controlling the final abscission. We questioned whether, similar to established factors, JADE1S is targeted to the central spindle structures in anaphase. Indeed, in cells transitioning from mitosis to cytokinesis, JADE1S was sequentially targeted to early midzone, midbody flanking zone, and midbody. The step-wise increase of JADE1S expression in midzone and midbody of synchronously dividing cells suggested protein recruitment. The increase of late cytokinesis arrest caused by recombinant JADE1S correlated with increased expression in midbody. Spatial analysis of the members of the chromatin passenger complex, microtubule associated proteins, and centralspindlin, revealed transient co-localization with JADE1S and mapped JADE1S within the cytokinesis bridge.Deletion of the two PHD zinc fingers inactivated JADE1S ability to arrest cells in late cytokinesis but did not affect its midbody localization. Thus, PHD zinc fingers are required for JADE1S cytokinesis delay but not for midbody targeting. Recombinant HBO1 protein decreased the proportion of late cytokinesis cells, prevented late cytokinesis arrest by JADE1S as well as its midbody localization. Enzyme inactive HBO1 mutant recapitulated the wild type phenotype. The results demonstrate antagonistic relationship and suggest HBO1-mediated midbody dislocation of JADE1S. Our study supports the role of JADE1S in cytokinesis delay and implicates protein partners.
Mycobacterium tuberculosisinfection elevates SLIT2 expression to modulate oxidative stress responses in macrophages
Authors: Borbora Salik Miskat , Bhatt Sneha , Balaji Kithiganahalli Narayanaswamy 
Published: October 2022

AbstractMycobacterium tuberculosis (Mtb), the causative agent of the pulmonary ailment, tuberculosis (TB), continues to thrive owing to a disorganized immune response against it by the host. Among other factors, the rewiring of distinct host signaling pathways is effectuated by the intracellular bacterium, resulting in pathogen-favorable outcomes. Oxidative stress build-up is a key cellular manifestation that occurs during mycobacterial infection. Enhanced oxidative stress is brought about by the cumulative effect of elevated reactive oxygen species generation as well as the inept ability of the cell to mitigate ROS levels. Here, we report the increased expression of the neuronal ligand, SLIT2, during mycobacterial infection in macrophages. By employing loss of function analysis using specific inhibitors, we attribute the heightened expression of SLIT2 to the Mtb-mediated phosphorylation of the p38/JNK pathways. Also, using chromatin immunoprecipitation (ChIP) analysis, we found reduced levels of the repressive H3K27me3 signature on the Slit2 promoter during mycobacterial infection. Furthermore, SLIT2 was found to promote the expression of cellular pantetheinase, Vanin1 (VNN1), that contributed to copious levels of ROS within the macrophage cellular milieu. Thus, we dissect essential molecular details leading to the robust expression of SLIT2 during Mtb infection while outlining the potential consequences of SLIT2 upregulation in infected macrophages.Graphical abstract
TPL2 kinase activity regulates microglial inflammatory responses and promotes neurodegeneration in tauopathy mice
Authors: Wang Yuanyuan , Wu Tiffany , Tsai Ming-Chi , Rezzonico Mitchell G , Abdel-Haleem Alyaa M , Xie Luke , Gandham Vineela D , Ngu Hai , Stark Kimberly , Glock Caspar , Xu Daqi , Foreman Oded , Friedman Brad A , Sheng Morgan , Hanson Jesse E 
Published: October 2022

AbstractTPL2 (MAP3K8) is a central signaling node in the inflammatory response of peripheral immune cells. We find that TPL2 kinase activity modulates microglial cytokine release and is required for microglia-mediated neuron deathin vitro. In acutein vivoneuroinflammation settings, TPL2 kinase activity regulates microglia activation states and brain cytokine levels. In a tauopathy model of chronic neurodegeneration, loss of TPL2 kinase activity reduces neuroinflammation and rescues synapse loss, brain volume loss, and behavioral deficits. Single-cell RNAseq analysis indicates protection in the tauopathy model was associated with reductions in activated microglia subpopulations as well as infiltrating peripheral immune cells. Overall, using various models, we find that TPL2 kinase activity can promote multiple harmful consequences of microglial activation in the brain including cytokine release, iNOS induction, astrocyte activation, and immune cell infiltration. Consequently, inhibiting TPL2 kinase activity could represent a potential therapeutic strategy in neurodegenerative conditions.
Natural alleles at theDoalocus underpin evolutionary changes inDrosophilalifespan and fecundity
Authors: Hoedjes Katja M. , Kostic Hristina , Keller Laurent , Flatt Thomas 
Published: October 2022

Abstract‘Evolve and resequence’ (E&R) studies inDrosophila melanogasterhave identified many candidate loci underlying the evolution of ageing and life history, but experiments that validate the effects of such candidates remain rare. In a recent E&R study we have identified several alleles of the LAMMER kinaseDarkener of apricot(Doa) as candidates for evolutionary changes in lifespan and fecundity. Here, we use two complementary approaches to confirm a functional role ofDoain life-history evolution. First, we used transgenic RNAi to study the effects ofDoaat the whole-gene level. Ubiquitous silencing of expression in adult flies reduced both lifespan and fecundity, indicating pleiotropic effects. Second, to characterize segregating variation atDoa, we examined four candidate single nucleotide polymorphisms (SNPs;Doa-1, −2, −3, −4) using a genetic association approach. Three candidate SNPs had effects that were qualitatively consistent with expectations based on our E&R study:Doa-2pleiotropically affected both lifespan and late-life fecundity;Doa-1affected lifespan (but not fecundity); andDoa-4affected late-life fecundity (but not lifespan). Finally, the last candidate allele (Doa-3) also affected lifespan, but in the opposite direction than predicted.
Computational Prediction of Binding Affinities of Human Angiotensin Converting Enzyme-2 with SARS-CoV-2 Spike Protein Variants: Omicron Variants and Potentially Deleterious Mutations
Authors: Williams Alexander H. , Zhan Chang-Guo 
Published: October 2022

AbstractThe Omicron variant (BA.1) and its sub-variants of the SARS-CoV-2 virus which causes the COVID-19 disease continues to spread across the United States and the World at large. As new sub-variants of SARS-CoV-2 continue to proliferate, a reliable computational method of quickly determining the potential infectivity of these new variants is needed to assess their potential threat. In the present study, we have tested and validated an efficient computational protocol, which includes an efficient energy minimization and subsequent molecular mechanics/Poisson Boltzmann surface area (MM-PBSA) calculation of the binding free energy between the SARS-CoV-2 spike protein and human angiotensin converting enzyme-2 (ACE2), to predict the binding affinities of these spike/ACE2 complexes based upon the calculated binding free energies and a previously calibrated linear correlation relationship. The predicted binding affinities are in good agreement with available experimental data including those for Omicron variants, suggesting that the predictions based on this protocol should be reasonable. Further, we have investigated several hundred potential mutations of both the wildtype and Omicron variants of the SARS-CoV-2 spike protein. Based on the predicted binding affinity data, we have identified several mutations that have the potential to vastly increase the binding affinity of the spike protein to ACE2 within both the wildtype and Omicron variants.Author SummaryAs well known, the coronavirus responsible for COVID-19 disease enters human cells through its spike protein binding with a human receptor protein known as angiotensin converting enzyme-2. So, the binding affinity between the spike protein and angiotensin converting enzyme-2 contributes to the infectivity of the coronavirus and its variants. In this study, we demonstrated that a generally applicable, fast and easy-to-use computational protocol was able to accurately predict the binding affinity of angiotensin converting enzyme-2 with spike protein of the currently known variants of the coronavirus. Hence, we believe that this computational protocol may be used to reliably predict the binding affinity of angiotensin converting enzyme-2 with spike protein of new variants to be identified in the future. Using this computational protocol, we have further examined a number of possible single mutations on the spike protein of both the wildtype and Omicron variants and predicted their binding affinity with angiotensin converting enzyme-2, demonstrating that several mutations have the potential to vastly increase the binding affinity of the spike protein to angiotensin converting enzyme-2.