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The mammalian target of rapamycin (mTOR) signaling pathway integrates both intracellular and extracellular signals and serves as a central regulator of cell metabolism, growth, proliferation and survival. Discoveries that have been made over the last decade show that the mTOR pathway is activated during various cellular processes (e.g. tumor formation and angiogenesis, insulin resistance, adipogenesis and T-lymphocyte activation) and is deregulated in human diseases such as cancer and type 2 diabetes. These observations have attracted broad scientific and clinical interest in mTOR. This is highlighted by the growing use of mTOR inhibitors [rapamycin and its analogues (rapalogues)] in pathological settings, including the treatment of solid tumors, organ transplantation, coronary restenosis and rheumatoid arthritis. Here, we highlight and summarize the current understanding of how mTOR nucleates distinct multi-protein complexes, how intra- and extracellular signals are processed by the mTOR complexes, and how such signals affect cell metabolism, growth, proliferation and survival.The mTOR protein is a 289-kDa serine-threonine kinase that belongs to the phospho-inositide 3-kinase (PI3K)-related kinase family and is conserved throughout evolution. The poster depicts an overview of mTOR structural domains. mTOR nucleates at least two distinct multi-protein complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) (reviewed by Guertin and Sabatini, 2007).mTORC1 has five components: mTOR, which is the catalytic subunit of the complex; regulatory-associated protein of mTOR (Raptor); mammalian lethal with Sec13 protein 8 (mLST8, also known as GβL); proline-rich AKT substrate 40 kDa (PRAS40); and DEP-domain-containing mTOR-interacting protein (Deptor) (Peterson et al., 2009). The exact function of most of the mTOR-interacting proteins in mTORC1 still remains elusive. It has been proposed that Raptor might affect mTORC1 activity by regulating assembly of the complex and by recruiting substrates for mTOR (Hara et al., 2002; Kim et al., 2002). The role of mLST8 in mTORC1 function is also unclear, as deletion of this protein does not affect mTORC1 activity in vivo (Guertin et al., 2006). PRAS40 and Deptor have been characterized as distinct negative regulators of mTORC1 (Peterson et al., 2009; Sancak et al., 2007; Vander Haar et al., 2007). When the activity of mTORC1 is reduced, PRAS40 and Deptor are recruited to the complex, where they promote the inhibition of mTORC1. It was proposed that PRAS40 regulates mTORC1 kinase activity by functioning as a direct inhibitor of substrate binding (Wang et al., 2007). Upon activation, mTORC1 directly phosphorylates PRAS40 and Deptor, which reduces their physical interaction with mTORC1 and further activates mTORC1 signaling (Peterson et al., 2009; Wang et al., 2007).mTORC2 comprises six different proteins, several of which are common to mTORC1 and mTORC2: mTOR; rapamycin-insensitive companion of mTOR (Rictor); mammalian stress-activated protein kinase interacting protein (mSIN1); protein observed with Rictor-1 (Protor-1); mLST8; and Deptor. There is some evidence that Rictor and mSIN1 stabilize each other, establishing the structural foundation of mTORC2 (Frias et al., 2006; Jacinto et al., 2006). Rictor also interacts with Protor-1, but the physiological function of this interaction is not clear (Thedieck et al., 2007; Woo et al., 2007). Similar to its role in mTORC1, Deptor negatively regulates mTORC2 activity (Peterson et al., 2009); so far, Deptor is the only characterized endogenous inhibitor of mTORC2. Finally, mLST8 is essential for mTORC2 function, as knockout of this protein severely reduces the stability and the activity of this complex (Guertin et al., 2006).Now that many mTOR-interacting proteins have been identified, additional biochemical studies will be needed to clarify the functions of these proteins in mTOR signaling and their potential implications in health and disease. Below, we discuss current understanding of the functions of mTORC1 and mTORC2.mTORC1 positively regulates cell growth and proliferation by promoting many anabolic processes, including biosynthesis of proteins, lipids and organelles, and by limiting catabolic processes such as autophagy. Much of the knowledge about mTORC1 function comes from the use of the bacterial macrolide rapamycin. Upon entering the cell, rapamycin binds to FK506-binding protein of 12 kDa (FKBP12) and interacts with the FKBP12-rapamycin binding domain (FRB) of mTOR, thus inhibiting mTORC1 functions (reviewed by Guertin and Sabatini, 2007). In contrast to its effect on mTORC1, FKBP12-rapamycin cannot physically interact with or acutely inhibit mTORC2 (Jacinto et al., 2004; Sarbassov et al., 2004). On the basis of these observations, mTORC1 and mTORC2 have been respectively characterized as the rapamycin-sensitive and rapamycin-insensitive complexes. However, this paradigm might not be entirely accurate, as chronic rapamycin treatment can, in some cases, inhibit mTORC2 activity by blocking its assembly (Sarbassov et al., 2006). In addition, recent reports suggest that important mTORC1 functions are resistant to inhibition by rapamycin (Choo et al., 2008; Feldman et al., 2009; Garcia-Martinez et al., 2009; Thoreen et al., 2009).mTORC1 positively controls protein synthesis, which is required for cell growth, through various downstream effectors. mTORC1 promotes protein synthesis by phosphorylating the eukaryotic initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) and the p70 ribosomal S6 kinase 1 (S6K1). The phosphorylation of 4E-BP1 prevents its binding to eIF4E, enabling eIF4E to promote cap-dependent translation (reviewed by Richter and Sonenberg, 2005). The stimulation of S6K1 activity by mTORC1 leads to increases in mRNA biogenesis, cap-dependent translation and elongation, and the translation of ribosomal proteins through regulation of the activity of many proteins, such as S6K1 aly/REF-like target (SKAR), programmed cell death 4 (PDCD4), eukaryotic elongation factor 2 kinase (eEF2K) and ribosomal protein S6 (reviewed by Ma and Blenis, 2009). The activation of mTORC1 has also been shown to promote ribosome biogenesis by stimulating the transcription of ribosomal RNA through a process involving the protein phosphatase 2A (PP2A) and the transcription initiation factor IA (TIF-IA) (Mayer et al., 2004).Autophagy – that is, the sequestration of intra - cellular components within autophagosomes and their degradation by lysosomes – is a catabolic process that is important in organelle degradation and protein turnover. When nutrient availability is limited, the degradation of organelles and protein complexes through autophagy provides biological material to sustain anabolic processes such as protein synthesis and energy production. Studies have shown that mTORC1 inhibition increases autophagy, whereas stimulation of mTORC1 reduces this process (reviewed by Codogno and Meier, 2005). We have observed that mTORC1 controls autophagy through an unknown mechanism that is essentially insensitive to inhibition by rapamycin (Thoreen et al., 2009). It was recently shown by three independent groups that mTORC1 controls autophagy through the regulation of a protein complex composed of unc-51-like kinase 1 (ULK1), autophagy-related gene 13 (ATG13) and focal adhesion kinase family-interacting protein of 200 kDa (FIP200) (Ganley et al., 2009; Hosokawa et al., 2009; Jung et al., 2009). These studies have revealed that mTORC1 represses autophagy by phosphorylating and thereby repressing ULK1 and ATG13.The role of mTORC1 in regulating lipid synthesis, which is required for cell growth and proliferation, is beginning to be appreciated. It has been demonstrated that mTORC1 positively regulates the activity of sterol regulatory element binding protein 1 (SREBP1) (Porstmann et al., 2008) and of peroxisome proliferator-activated receptor-γ (PPARγ) (Kim and Chen, 2004), two transcription factors that control the expression of genes encoding proteins involved in lipid and cholesterol homeostasis. Blocking mTOR with rapamycin reduces the expression and the transactivation activity of PPARγ (Kim and Chen, 2004). The molecular mechanism of SREBP1 activation by mTORC1 is unknown. Additionally, rapamycin reduces the phosphorylation of lipin-1 (Huffman et al., 2002), a phosphatidic acid (PA) phosphatase that is involved in glycerolipid synthesis and in the coactivation of many transcription factors linked to lipid metabolism, including PPARγ, PPARα and PGC1-α. The precise impact of lipin-1 phosphorylation on lipid synthesis remains to be established.Mitochondrial metabolism and biogenesis are both regulated by mTORC1. Inhibition of mTORC1 by rapamycin lowers mitochondrial membrane potential, oxygen consumption and cellular ATP levels, and profoundly alters the mitochondrial phosphoproteome (Schieke et al., 2006). Recently, it has been observed that mitochondrial DNA copy number, as well as the expression of many genes encoding proteins involved in oxidative metabolism, are reduced by rapamycin and increased by mutations that activate mTORC1 signaling (Chen et al., 2008; Cunningham et al., 2007). Additionally, conditional deletion of Raptor in mouse skeletal muscle reduces the expression of genes involved in mitochondrial biogenesis (Bentzinger et al., 2008). Cunningham and colleagues have discovered that mTORC1 controls the transcriptional activity of PPARγ coactivator 1 (PGC1-α), a nuclear cofactor that plays a key role in mitochondrial biogenesis and oxidative metabolism, by directly altering its physical interaction with another transcription factor, namely yin-yang 1 (YY1) (Cunningham et al., 2007).mTORC1 integrates four major signals – growth factors, energy status, oxygen and amino acids – to regulate many processes that are involved in the promotion of cell growth. One of the most important sensors involved in the regulation of mTORC1 activity is the tuberous sclerosis complex (TSC), which is a heterodimer that comprises TSC1 (also known as hamartin) and TSC2 (also known as tuberin). TSC1/2 functions as a GTPase-activating protein (GAP) for the small Ras-related GTPase Rheb (Ras homolog enriched in brain). The active, GTP-bound form of Rheb directly interacts with mTORC1 to stimulate its activity (Long et al., 2005; Sancak et al., 2007). The exact mechanism by which Rheb activates mTORC1 remains to be determined. As a Rheb-specific GAP, TSC1/2 negatively regulates mTORC1 signaling by converting Rheb into its inactive GDP-bound state (Inoki et al., 2003; Tee et al., 2003). Consistent with a role of TSC1/2 in the negative regulation of mTORC1, inactivating mutations or loss of heterozygosity of TSC1/2 give rise to tuberous sclerosis, a disease associated with the presence of numerous benign tumors that are composed of enlarged and disorganized cells (reviewed by Crino et al., 2006).Growth factors stimulate mTORC1 through the activation of the canonical insulin and Ras signaling pathways. The stimulation of these pathways increases the phosphorylation of TSC2 by protein kinase B (PKB, also known as AKT) (Inoki et al., 2002; Potter et al., 2002), by extracellular-signal-regulated kinase 1/2 (ERK1/2) (Ma et al., 2005), and by p90 ribosomal S6 kinase 1 (RSK1) (Roux et al., 2004), and leads to the inactivation of TSC1/2 and thus to the activation of mTORC1. Additionally, AKT activation by growth factors can activate mTORC1 in a TSC1/2-independent manner by promoting the phosphorylation and dissociation of PRAS40 from mTORC1 (Sancak et al., 2007; Vander Haar et al., 2007; Wang et al., 2007).The binding of insulin to its cell-surface receptor promotes the tyrosine kinase activity of the insulin receptor, the recruitment of insulin receptor substrate 1 (IRS1), the production of phosphatidylinositol (3,4,5)-triphosphate [PtdIns(3,4,5)P3] through the activation of PI3K, and the recruitment and activation of AKT at the plasma membrane. In many cell types, activation of mTORC1 strongly represses the PI3K-AKT axis upstream of PI3K. Activation of S6K1 by mTORC1 promotes the phosphorylation of IRS1 and reduces its stability (reviewed by Harrington et al., 2005). This auto-regulatory pathway, characterized as the S6K1-dependent negative feedback loop, has been shown to have profound implications for both metabolic diseases and tumorigenesis (reviewed by Manning, 2004). Other pathways that are independent of IRS1 are also likely to contribute to the retro-inhibition of mTORC1. For example, loss of TSC1/2 suppresses platelet-derived growth factor receptor (PDGFR) expression in a rapamycin-sensitive manner (Zhang et al., 2007). How mTOR signaling controls PDGFR expression remains to be determined.The energy status of the cell is signaled to mTORC1 through AMP-activated protein kinase (AMPK), a master sensor of intracellular energy status (reviewed by Hardie, 2007). In response to energy depletion (low ATP:ADP ratio), AMPK is activated and phosphorylates TSC2, which increases the GAP activity of TSC2 towards Rheb and reduces mTORC1 activation (Inoki et al., 2003). Additionally, AMPK can reduce mTORC1 activity in response to energy depletion by directly phosphorylating Raptor (Gwinn et al., 2008).Oxygen levels affect mTORC1 activity through multiple pathways (reviewed by Wouters and Koritzinsky, 2008). Under conditions of mild hypoxia, the reduction in ATP levels activates AMPK, which promotes TSC1/2 activation and inhibits mTORC1 signaling as described in the previous section (Arsham et al., 2003; Liu et al., 2006). Hypoxia can also activate TSC1/2 through transcriptional regulation of DNA damage response 1 (REDD1) (Brugarolas et al., 2004; Reiling and Hafen, 2004). REDD1 blocks mTORC1 signaling by releasing TSC2 from its growth-factor-induced association with 14-3-3 proteins (DeYoung et al., 2008). This ability of REDD1 to reduce mTORC1 signaling by disrupting the interaction of TSC2 and 14-3-3 has probably evolved to limit energy-consuming processes when oxygen, but not growth factors, is scarce. Additionally, promyelocytic leukemia (PML) tumor suppressor and BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) reduce mTORC1 signaling during hypoxia by disrupting the interaction between mTOR and its positive regulator Rheb (Bernardi et al., 2006; Li et al., 2007).Amino acids represent a strong signal that positively regulates mTORC1 (reviewed by Guertin and Sabatini, 2007). It was recently shown that leucine, an essential amino acid required for mTORC1 activation, is transported into cells in a glutamine-dependent fashion (Nicklin et al., 2009). Glutamine, which is imported into cells through SLC1A5 [solute carrier family 1 (neutral amino acid transporter) member 5], is exchanged to import leucine via a heterodimeric system composed of SLC7A5 [antiport solute carrier family 7 (cationic amino acid transporter, y+ system, member 5] and SLC3A2 [solute carrier family 3 (activators of dibasic and neutral amino acid transport) member 2]. The mechanism by which intracellular amino acids then signal to mTORC1 remained obscure for many years. The activation of mTORC1 by amino acids is known to be independent of TSC1/2, because the mTORC1 pathway remains sensitive to amino acid deprivation in cells that lack TSC1 or TSC2 (Nobukuni et al., 2005). Some studies have implicated human vacuolar protein-sorting-associated protein 34 (VPS34) in nutrient sensing (Nobukuni et al., 2005); however, the precise role of human VPS34 in this process still remains to be established (Juhasz et al., 2008).Recently, two independent teams, including ours, have shown that the Rag proteins, a family of four related small GTPases, interact with mTORC1 in an amino acid-sensitive manner and are necessary for the activation of the mTORC1 pathway by amino acids (Kim et al., 2008; Sancak et al., 2008). In the presence of amino acids, Rag proteins bind to Raptor and promote the relocalization of mTORC1 from discrete locations throughout the cytoplasm to a perinuclear region that contains its activator Rheb (Sancak et al., 2008). The physical dissociation of mTORC1 and Rheb with amino acid deprivation might explain why activators of Rheb, such as growth factors, cannot stimulate mTORC1 signaling in the absence of amino acids.In addition to the key signals described above, other cellular conditions and signals, such as genotoxic stress, inflammation, Wnt ligand and PA, have all been shown to regulate mTORC1 signaling. Genotoxic stress reduces mTORC1 activity through many mechanisms. For instance, the activation of p53 in response to DNA damage rapidly activates AMPK through an unknown process, which in turn phosphorylates and thereby activates TSC2 (Feng et al., 2005). Additionally, p53 negatively controls mTORC1 signaling by increasing the transcription of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and TSC2, two negative regulators of the pathway (Feng et al., 2005; Stambolic et al., 2001). Inflammatory mediators also signal to mTORC1 via the TSC1/2 complex. Pro-inflammatory cytokines, such as TNFα, activate IκB kinase-β (IKKβ), which physically interacts with and inactivates TSC1, leading to mTORC1 activation (Lee et al., 2007). This positive relationship between inflammation and mTORC1 activation is thought to be important in tumor angiogenesis (Lee et al., 2007) and in the development of insulin resistance (Lee et al., 2008). Wnt signaling also increases mTORC1 activity through the inactivation of TSC1/2. Stimulation of the Wnt pathway inhibits glycogen synthase kinase 3 (GSK3), a kinase that promotes TSC1/2 activity by directly phosphorylating TSC2 (Inoki et al., 2006). Finally, PA has been identified as another activator of mTORC1. Many groups have shown that exogenous PA or overexpression of PA-producing enzymes such as phospholipase D1 (PLD1) and PLD2 significantly increases mTORC1 signaling (reviewed by Foster, 2007). A recent study suggests that PA affects mTOR signaling by facilitating the assembly of mTOR complexes, or stabilizing the complexes (Toschi et al., 2009).In contrast to mTORC1, for which many upstream signals and cellular functions have been defined (see above), relatively little is known about mTORC2 biology. The early lethality caused by the deletion of mTORC2 components in mice, as well as the absence of mTORC2 inhibitors, have complicated the study of this protein complex. Nonetheless, many important discoveries have been made over the last few years. Using various genetic approaches, it has been demonstrated that mTORC2 plays key roles in various biological processes, including cell survival, metabolism, proliferation and cytoskeleton organization. The role of mTORC2 in these processes is discussed in more detail below.Cell survival, metabolism and proliferation are all highly dependent on the activation status of AKT, which positively regulates these processes through the phosphorylation of various effectors (reviewed by Manning and Cantley, 2007). Full activation of AKT requires its phosphorylation at two sites: Ser308, by phosphoinositide-dependent kinase 1 (PDK1), and Ser473, by a kinase that remained unidentified for many years, but was demonstrated to be mTORC2 by our group in 2005 (Sarbassov et al., 2005). Other studies have subsequently observed that ablation of various mTORC2 components specifically blocks AKT phosphorylation at Ser473 and the downstream phosphorylation of some, but not all, AKT substrates (Guertin et al., 2006; Jacinto et al., 2006). Inhibition of AKT following mTORC2 depletion reduces the phosphorylation of, and therefore activates, the forkhead box protein O1 (FoxO1) and FoxO3a transcription factors, which control the expression of genes involved in stress resistance, metabolism, cell-cycle arrest and apoptosis (reviewed by Calnan and Brunet, 2008). By contrast, the phosphorylation state of TSC2 and GSK3 is not affected by mTORC2 inactivation. Recently, serum- and glucocorticoid-induced protein kinase 1 (SGK1), which shares homology with AKT, was also shown to be regulated by mTORC2 (Garcia-Martinez and Alessi, 2008). In contrast to AKT, which a activity when mTORC2 is activity is these and AKT and FoxO3a on common it is that the lack of activity in cells is for the inhibition of phosphorylation of and regulates organization. Many independent groups have observed that mTORC2 components affects and cell (Jacinto et al., 2004; Sarbassov et al., 2004). These studies have that mTORC2 controls the cytoskeleton by promoting protein kinase phosphorylation of and its relocalization to focal and the of and The molecular mechanism by which mTORC2 regulates these processes has not been determined.The signaling pathways that to mTORC2 activation are not well growth factors mTORC2 kinase activity and AKT phosphorylation at Ser473, they are to be a signal for regulating this pathway (reviewed by Guertin and Sabatini, 2007). AKT is at the cell membrane through the binding of to its homology Under these is also recruited to the membrane through its domain and phosphorylates AKT at (reviewed by and Alessi, 2001). the mTORC2 mSIN1 a domain at its that mSIN1 can promote the of mTORC2 to the membrane and the phosphorylation of AKT at is needed to this and to other cellular signals that a role in the regulation of the last knowledge of the mTOR signaling pathway has enabling to the mechanism of diseases such as cancer and type 2 diabetes. these our understanding of this signaling is from and many important to be For example, how is mTORC2 regulated and which biological processes does it How are the mTORC1 and mTORC2 signaling pathways with each are the functions of these complexes in and and are the implications of their or in health and additional mTOR complexes that regulate other biological to these important will our understanding of cellular and will also the development of to many human

GREX-PLUS (Galaxy Reionization EXplorer and PLanetary Universe Spectrometer) is a mission candidate for a JAXA strategic L-class mission to be launched in the 2030s. Its primary science goals are two-fold: galaxy formation and evolution, and planetary system formation and evolution. The GREX-PLUS spacecraft will carry a telescope with a 1 m primary mirror aperture cooled down to 50 K. The two science instruments will be onboard: a wide-field camera in the 2--8 $μ$m wavelength band and a high-resolution spectrometer with a wavelength resolution of 30,000 in the 10--18 $μ$m band. The GREX-PLUS wide-field camera aims to detect the first generation of galaxies at redshift $z>15$. The GREX-PLUS high-resolution spectrometer aims to identify the location of the water ``snowline'' in protoplanetary disks. Both instruments will provide unique datasets for a broad range of scientific topics, including galaxy mass assembly, the origin of supermassive blackholes, infrared background radiation, molecular spectroscopy in the interstellar medium, transit spectroscopy of exoplanet atmospheres, planetary atmospheres in the Solar System, and so on. This document is the second version of a collect

Current definitions of Information Science are inadequate to comprehensively describe the nature of its field of study and for addressing the problems that are arising from intelligent technologies. The ubiquitous rise of artificial intelligence applications and their impact on society demands the field of Information Science acknowledge the sociotechnical nature of these technologies. Previous definitions of Information Science over the last six decades have inadequately addressed the environmental, human, and social aspects of these technologies. This perspective piece advocates for an expanded definition of Information Science that fully includes the sociotechnical impacts information has on the conduct of research in this field. Proposing an expanded definition of Information Science that includes the sociotechnical aspects of this field should stimulate both conversation and widen the interdisciplinary lens necessary to address how intelligent technologies may be incorporated into society and our lives more fairly.

The Vera C. Rubin Observatory's Legacy Survey of Space and Time (LSST) will produce unprecedented volumes of heterogeneous astronomical data (images, catalogs, and alerts) that challenge traditional analysis pipelines. The LSST Dark Energy Science Collaboration (DESC) aims to derive robust constraints on dark energy and dark matter from these data, requiring methods that are statistically powerful, scalable, and operationally reliable. Artificial intelligence and machine learning (AI/ML) are already embedded across DESC science workflows, from photometric redshifts and transient classification to weak lensing inference and cosmological simulations. Yet their utility for precision cosmology hinges on trustworthy uncertainty quantification, robustness to covariate shift and model misspecification, and reproducible integration within scientific pipelines. This white paper surveys the current landscape of AI/ML across DESC's primary cosmological probes and cross-cutting analyses, revealing that the same core methodologies and fundamental challenges recur across disparate science cases. Since progress on these cross-cutting challenges would benefit multiple probes simultaneously, we ide

The large instantaneous sensitivity, a wide frequency coverage and flexible observation modes with large number of beams in the sky are the main features of the SKA observatory's two telescopes, the SKA-Low and the SKA-Mid, which are located on two different continents. Owing to these capabilities, the SKAO telescopes are going to be a game-changer for radio astronomy in general and pulsar astronomy in particular. The eleven articles in this special issue on pulsar science with the SKA Observatory describe its impact on different areas of pulsar science. In this lead article, a brief description of the two telescopes highlighting the relevant features for pulsar science is presented followed by an overview of each accompanying article, exploring the inter-relationship between different pulsar science use cases.

Mauve is a low-cost small satellite developed and operated by Blue Skies Space Ltd. The payload features a 13 cm telescope connected with a fibre that feeds into a UV-Vis spectrometer. The detector covers the 200-700 nm range in a single shot, obtaining low resolution spectra at R~20-65. Mauve has launched on 28th November 2025, reaching a 510 km Low-Earth Sun-synchronous orbit. The satellite will enable UV and visible observations of a variety of stellar objects in our Galaxy, filling the gaps in the ultraviolet space-based data. The researchers that have already joined the mission have defined the science themes, observational strategy and targets that Mauve will observe in the first year of operations. To date 10 science themes have been developed by the Mauve science collaboration for year 1, with observational strategies that include both long duration monitoring and short cadence snapshots. Here, we describe these themes and the science that Mauve will undertake in its first year of operations.

Large language models (LLMs) have exhibited exceptional capabilities in natural language understanding and generation, image recognition, and multimodal tasks, charting a course towards AGI and emerging as a central issue in the global technological race. This manuscript conducts a comprehensive review of the core technologies that support LLMs from a user standpoint, including prompt engineering, knowledge-enhanced retrieval augmented generation, fine tuning, pretraining, and tool learning. Additionally, it traces the historical development of Science of Science (SciSci) and presents a forward looking perspective on the potential applications of LLMs within the scientometric domain. Furthermore, it discusses the prospect of an AI agent based model for scientific evaluation, and presents new research fronts detection and knowledge graph building methods with LLMs.

We investigate the development of scientific content knowledge of volunteers participating in online citizen science projects in the Zooniverse (www.zooniverse.org), including the astronomy projects Galaxy Zoo (www.galaxyzoo.org) and Planet Hunters (www.planethunters.org). We use econometric methods to test how measures of project participation relate to success in a science quiz, controlling for factors known to correlate with scientific knowledge. Citizen scientists believe they are learning about both the content and processes of science through their participation. Won't don't directly test the latter, but we find evidence to support the former - that more actively engaged participants perform better in a project-specific science knowledge quiz, even after controlling for their general science knowledge. We interpret this as evidence of learning of science content inspired by participation in online citizen science.

Data science and technology offer transformative tools and methods to science. This review article highlights latest development and progress in the interdisciplinary field of data-driven plasma science (DDPS). A large amount of data and machine learning algorithms go hand in hand. Most plasma data, whether experimental, observational or computational, are generated or collected by machines today. It is now becoming impractical for humans to analyze all the data manually. Therefore, it is imperative to train machines to analyze and interpret (eventually) such data as intelligently as humans but far more efficiently in quantity. Despite the recent impressive progress in applications of data science to plasma science and technology, the emerging field of DDPS is still in its infancy. Fueled by some of the most challenging problems such as fusion energy, plasma processing of materials, and fundamental understanding of the universe through observable plasma phenomena, it is expected that DDPS continues to benefit significantly from the interdisciplinary marriage between plasma science and data science into the foreseeable future.

Deep learning has enabled major advances across most areas of artificial intelligence research. This remarkable progress extends beyond mere engineering achievements and holds significant relevance for the philosophy of cognitive science. Deep neural networks have made significant strides in overcoming the limitations of older connectionist models that once occupied the centre stage of philosophical debates about cognition. This development is directly relevant to long-standing theoretical debates in the philosophy of cognitive science. Furthermore, ongoing methodological challenges related to the comparative evaluation of deep neural networks stand to benefit greatly from interdisciplinary collaboration with philosophy and cognitive science. The time is ripe for philosophers to explore foundational issues related to deep learning and cognition; this perspective paper surveys key areas where their contributions can be especially fruitful.

Data Science is a modern Data Intelligence practice, which is the core of many businesses and helps businesses build smart strategies around to deal with businesses challenges more efficiently. Data Science practice also helps in automating business processes using the algorithm, and it has several other benefits, which also deliver in a non-profitable framework. In regards to data science, three key components primarily influence the effective outcome of a data science project. Those are 1.Availability of Data 2.Algorithm 3.Processing power or infrastructure

The Large Synoptic Survey Telescope (LSST) will enable revolutionary studies of galaxies, dark matter, and black holes over cosmic time. The LSST Galaxies Science Collaboration has identified a host of preparatory research tasks required to leverage fully the LSST dataset for extragalactic science beyond the study of dark energy. This Galaxies Science Roadmap provides a brief introduction to critical extragalactic science to be conducted ahead of LSST operations, and a detailed list of preparatory science tasks including the motivation, activities, and deliverables associated with each. The Galaxies Science Roadmap will serve as a guiding document for researchers interested in conducting extragalactic science in anticipation of the forthcoming LSST era.

The Aryabhatta Research Institute of Observational Sciences (ARIES), a premier autonomous research institute under the Department of Science and Technology, Government of India has a legacy of about seven decades with contributions made in the field of observational sciences namely atmospheric and astrophysics. The Survey of India used a location at ARIES, determined with an accuracy of better than 10 meters on a world datum through institute participation in a global network of Earth artificial satellites imaging during late 1950. Taking advantage of its high-altitude location, ARIES, for the first time, provided valuable input for climate change studies by long term characterization of physical and chemical properties of aerosols and trace gases in the central Himalayan regions. In astrophysical sciences, the institute has contributed precise and sometime unique observations of the celestial bodies leading to a number of discoveries. With the installation of the 3.6 meter Devasthal optical telescope in the year 2015, India became the only Asian country to join those few nations of the world who are hosting 4 meter class optical telescopes. This telescope, having advantage of geog

Researchers may be tempted to attract attention through poetic titles for their publications, but would this be mistaken in some fields? Whilst poetic titles are known to be common in medicine, it is not clear whether the practice is widespread elsewhere. This article investigates the prevalence of poetic expressions in journal article titles 1996-2019 in 3.3 million articles from all 27 Scopus broad fields. Expressions were identified by manually checking all phrases with at least 5 words that occurred at least 25 times, finding 149 stock phrases, idioms, sayings, literary allusions, film names and song titles or lyrics. The expressions found are most common in the social sciences and the humanities. They are also relatively common in medicine, but almost absent from engineering and the natural and formal sciences. The differences may reflect the less hierarchical and more varied nature of the social sciences and humanities, where interesting titles may attract an audience. In engineering, natural science and formal science fields, authors should take extra care with poetic expressions, in case their choice is judged inappropriate. This includes interdisciplinary research overlapp

The search for extraterrestrial life in the Solar System and beyond is a key science driver in astrobiology, planetary science, and astrophysics. A critical step is the identification and characterization of potential habitats, both to guide the search and to interpret its results. However, a well-accepted, self-consistent, flexible, and quantitative terminology and method of assessment of habitability are lacking. Our paper fills this gap based on a three year-long study by the NExSS Quantitative Habitability Science Working Group. We reviewed past studies of habitability, but find that the lack of a universally valid definition of life prohibits a universally applicable definition of habitability. A more nuanced approach is needed. We introduce a quantitative habitability assessment framework (QHF) that enables self-consistent, probabilistic assessment of the compatibility of two models: First, a habitat model, which describes the probability distributions of key conditions in the habitat. Second, a viability model, which describes the probability that a metabolism is viable given a set of environmental conditions. We provide an open-source implementation of this framework and fo

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The Open Science Grid (OSG) includes work to enable new science, new scientists, and new modalities in support of computationally based research. There are frequently significant sociological and organizational changes required in transformation from the existing to the new. OSG leverages its deliverables to the large scale physics experiment member communities to benefit new communities at all scales through activities in education, engagement and the distributed facility. As a partner to the poster and tutorial at SciDAC 2008, this paper gives both a brief general description and some specific examples of new science enabled on the OSG. More information is available at the OSG web site: (http://www.opensciencegrid.org).

SPIRou is a near-infrared (nIR) spectropolarimeter / velocimeter proposed as a new-generation instrument for CFHT. SPIRou aims in particular at becoming world-leader on two forefront science topics, (i) the quest for habitable Earth-like planets around very- low-mass stars, and (ii) the study of low-mass star and planet formation in the presence of magnetic fields. In addition to these two main goals, SPIRou will be able to tackle many key programs, from weather patterns on brown dwarf to solar-system planet atmospheres, to dynamo processes in fully-convective bodies and planet habitability. The science programs that SPIRou proposes to tackle are forefront (identified as first priorities by most research agencies worldwide), ambitious (competitive and complementary with science programs carried out on much larger facilities, such as ALMA and JWST) and timely (ideally phased with complementary space missions like TESS and CHEOPS). SPIRou is designed to carry out its science mission with maximum efficiency and optimum precision. More specifically, SPIRou will be able to cover a very wide single-shot nIR spectral domain (0.98-2.35 μm) at a resolving power of 73.5K, providing unpolariz

Throughout history, everyday people have contributed to science through a myriad of volunteer activities. This early participation required training and often involved mentorship from scientists or senior citizen scientists (or, as they were often called, gentleman scientists). During this learning process, participants learned how they and their data would be used both to advance science, and in some cases, advance the careers of professional collaborators. Modern, online citizen science, allows participation with just a few clicks, and people may participate without understanding what they are contributing to. Too often, they happily see what they are doing as the privilege of painting Tom Sawyer's fence without realizing they are actually being used as merely a means to a scientific end. This paper discusses the ethical dilemmas that plague modern citizen science, including: the issues of informed consent, such as not requiring logins; the issues of coercion inherent in mandatory classroom assignments requiring data submission; and the issues of using people merely as a means to an end that are inherent in technonationalism, and projects that do not provide utility to the users