Miracle-dz/UniFAR-FTUs huggingface dataset:
Immediate and Sustained Decrease in Smoking Urges After Acute Insular Cortex Damage

Introduction Smoking urges are fundamental aspects of nicotine dependence that contribute significantly to drug use and postquit relapse. Recent evidence has indicated that damage to the insular cortex disrupts smoking behaviors and claims to reduce urges associated with nicotine use, although tools that assess urge have yet to be used to validate these findings. We examined the effect of insular versus non-insular damage on urge using a well-accepted urge scale. Methods This 3-month observational prospective cohort study consisted of 156 current smokers hospitalized for acute ischemic stroke (38 with insular infarctions, 118 with non-insular infarctions). During hospitalization, the Questionnaire of Smoking Urges (QSU)-brief was assessed retrospectively based on experiences before the stroke (baseline, T0), prospectively immediately following the stroke (T1) and once more via telephone at 3-month follow-up (T2), with higher scores indicating greater urge. Bivariate statistics and multivariable linear regression were used to evaluate differences in QSU-brief scores, relative to baseline, between exposure groups, controlling for age, baseline dependence, stroke severity, use of nicotine replacement, and damage to other mesocorticolimbic regions. Results A greater reduction in QSU-brief score was seen in the insular group compared to the non-insular group from T0 to T1 (covariate-adjusted difference in means of -1.15, 95% CI: -1.85, -0.44) and similarly from T0 to T2 (covariate-adjusted difference in means of -0.93, 95% CI: -1.79, -0.07). Conclusions These findings confirm the potential role of the insula in regulating nicotine-induced urges and support the growing evidence of its novelty as a key target for smoking cessation interventions. Implications Human lesioning studies that evaluate the insula's involvement in maintaining nicotine addiction make inferences of the insula's role in decreasing urge, but do not use validated instruments that directly assess urges. This study corroborates prior findings using the continuous Questionnaire of Smoking Urges to quantify changes in urge from before lesion onset to immediate and 3-month follow-up time points.
Dopamine D2 receptor availability is linked to hippocampal–caudate functional connectivity and episodic memory

Significance Cognitive functioning depends in part on dopamine neurotransmission in the brain. Research implicates the dopamine D1 receptor family in cognitive functions linked to the prefrontal cortex, such as working memory. The dopamine D2 receptor family has also been linked to cognition, but it remains unclear to which cognitive functions it is specifically related. We examined the relation of D2 receptors to episodic memory, working memory, and speed of processing. D2 receptors in the caudate and hippocampus were related to episodic memory and modulated caudate–hippocampal functional connections. These findings link the dopamine D2 system to hippocampus-based cognitive functions. D1 and D2 dopamine receptors (D1DRs and D2DRs) may contribute differently to various aspects of memory and cognition. The D1DR system has been linked to functions supported by the prefrontal cortex. By contrast, the role of the D2DR system is less clear, although it has been hypothesized that D2DRs make a specific contribution to hippocampus-based cognitive functions. Here we present results from 181 healthy adults between 64 and 68 y of age who underwent comprehensive assessment of episodic memory, working memory, and processing speed, along with MRI and D2DR assessment with [11C]raclopride and PET. Caudate D2DR availability was positively associated with episodic memory but not with working memory or speed. Whole-brain analyses further revealed a relation between hippocampal D2DR availability and episodic memory. Hippocampal and caudate D2DR availability were interrelated, and functional MRI-based resting-state functional connectivity between the ventral caudate and medial temporal cortex increased as a function of caudate D2DR availability. Collectively, these findings indicate that D2DRs make a specific contribution to hippocampus-based cognition by influencing striatal and hippocampal regions, and their interactions.
Stacked charge stripes in the quasi-2D trilayer nickelate La4Ni3O8

Significance Competition between localized and itinerant electrons in highly correlated materials can lead to myriad insulating ground states, including spatially inhomogeneous but ordered charge superlattices. In layered transition metal oxides, such charge order can take the form of stripes, which typically arrange themselves in staggered formations to reduce Coulomb repulsion. Having achieved single-crystal growth of the layered nickelate La4Ni3O8, we show that its heretofore incompletely understood phase transition is associated with charge stripe ordering. We find that the stripes are stacked directly on top of one another within nickel oxide trilayers but staggered between successive trilayers. A unique, paradoxical ground state results, in which the electrostatic building principle is respected at long range but violated at short range. The quasi-2D nickelate La4Ni3O8 (La-438), consisting of trilayer networks of square planar Ni ions, is a member of the so-called T′ family, which is derived from the Ruddlesden–Popper (R-P) parent compound La4Ni3O10−x by removing two oxygen atoms and rearranging the rock salt layers to fluorite-type layers. Although previous studies on polycrystalline samples have identified a 105-K phase transition with a pronounced electronic and magnetic response but weak lattice character, no consensus on the origin of this transition has been reached. Here, we show using synchrotron X-ray diffraction on high-pO2 floating zone-grown single crystals that this transition is associated with a real space ordering of charge into a quasi-2D charge stripe ground state. The charge stripe superlattice propagation vector, q = (2/3, 0, 1), corresponds with that found in the related 1/3-hole doped single-layer R-P nickelate, La5/3Sr1/3NiO4 (LSNO-1/3; Ni2.33+), with orientation at 45° to the Ni-O bonds. The charge stripes in La-438 are weakly correlated along c to form a staggered ABAB stacking that reduces the Coulomb repulsion among the stripes. Surprisingly, however, we find that the charge stripes within each trilayer of La-438 are stacked in phase from one layer to the next, at odds with any simple Coulomb repulsion argument.
International Journal of Information Management Strategic Knowledge Management, Innovation and Performance

Our aim is to shed light on the consequences of knowledge management (KM) strategies on firm's innovation and corporate performance. Organisations are not aware of the real implications that KM may have. Based on an empirical study consisted of 310 Spanish organisations and structural equations modelling , results show that both KM strategies (codification and personalisation) impacts on innovation and organisational performance directly and indirectly (through an increase on innovation capability). Also, findings demonstrate a different effect of KM strategies on diverse dimensions of organisational performance. Our conclusions may help academics and managers in designing KM strategic programs in order to achieve higher innovation, effectiveness, efficiency and profitability.
Assessment of pain and disability in patients with chronic low back pain: Reliability and construct validity of the Turkish version of the Quebec Back Pain Disability Scale and Pain Disability Index

Objectives: The objective of this study was to test the reliability and validity of the Turkish version of the Quebec Back Pain Disability Scale (QBPDS) and Pain Disability Index (PDI) as well as the retainment of the psychometric properties of the original versions. The importance of the region-specific functional measures on patients with chronic low back pain was also assessed. Methods: Eighty-three patients with chronic low back pain were enrolled in the study. The QBPDS, the PDI and The Hospital Anxiety and Depression Scale (HADS) were filled by all subjects. Reliability was determined by internal consistency. Internal consistency was measured by calculating Cronbach's alpha and item-total correlation. Validity was examined by correlating the QBPDS and PDI scores to external criteria scores at a single point in time, defined as cross-sectional construct validity. Results: Cronbach's alpha value for QBPDS and PDI was found 0.93 and 0.84 respectively, which were both statistically significant ( p< 0.0001). The item-total correlations of QBPDS varied between 0.28 and 0.76, and that of PDI varied between 0.30 and 0.73. The cross-sectional construct validity coefficients of QBPDS were 0.63 for PDI, 0.46 for Visual Analogue Scale (VAS), 0.28 and 0.16 for HADS. Correlation coefficients of PDI were 0.49, and those of VAS and HADS were 0.36 and 0.24 respectively. Conclusion: Our results are in accordance with the previous findings of the English and French versions of the QBPDS and English version of the PDI, indicating that these functional scales are valid and reliable. However, due to the considerable overlap between generic and region-specific functional instruments, the use of both scales is not necessary. We conclude that the QBPDS and PDI both measure predominantly functional status in patients with chronic low back pain.
Pericyte–fibroblast transition promotes tumor growth and metastasis

Significance We show that vascular pericytes significantly contribute to cancer invasion and metastasis by the mechanism of the pericyte–fibroblast transition (PFT). This study proposes this concept and indicates the vascular pericyte’s role. Vascular pericytes were considered to remodel tumor vessels toward a mature phenotype. However, once dissociated from tumor vessels their functions within the tumor tissue are not known. In the present study, we show that pericytes, once detached from tumor microvasculatures, underwent differentiation to become stromal fibroblasts, which are known to contribute to tumor invasion and metastasis. Our results show that vascular pericytes are the important source of stromal fibroblasts and targeting PFT may offer a new treatment option in cancer metastasis. Vascular pericytes, an important cellular component in the tumor microenvironment, are often associated with tumor vasculatures, and their functions in cancer invasion and metastasis are poorly understood. Here we show that PDGF-BB induces pericyte–fibroblast transition (PFT), which significantly contributes to tumor invasion and metastasis. Gain- and loss-of-function experiments demonstrate that PDGF-BB-PDGFRβ signaling promotes PFT both in vitro and in in vivo tumors. Genome-wide expression analysis indicates that PDGF-BB–activated pericytes acquire mesenchymal progenitor features. Pharmacological inhibition and genetic deletion of PDGFRβ ablate the PDGF-BB–induced PFT. Genetic tracing of pericytes with two independent mouse strains, TN-AP-CreERT2:R26R-tdTomato and NG2-CreERT2:R26R-tdTomato, shows that PFT cells gain stromal fibroblast and myofibroblast markers in tumors. Importantly, coimplantation of PFT cells with less-invasive tumor cells in mice markedly promotes tumor dissemination and invasion, leading to an increased number of circulating tumor cells and metastasis. Our findings reveal a mechanism of vascular pericytes in PDGF-BB–promoted cancer invasion and metastasis by inducing PFT, and thus targeting PFT may offer a new treatment option of cancer metastasis.
Role of autologous mesenchymal stem cells associated with platelet‐rich plasma on healing of cutaneous wounds in diabetic mice

Background. Chronic cutaneous lesions affect 15% of human patients with diabetes, and the associated risk of limb amputations is 15–46 times greater than that of people with normal glycaemia. It is estimated that half of these limb amputations could be avoided by opportune treatment with somatic stem cells or platelet‐rich plasma (PRP).
International Journal of Information Management Improving Performance Aligning Business Analytics with Process Orientation

How to align business analytics with process orientation initiatives and how management can influence a synergistic accomplishment of these two elements in order to streamline organizational performance is a foremost managerial issue. By means of a quantitative research effort, a study was designed to investigate the relationships among these constructs. Empirical data were collected in 2011 from a survey of 368 large and mid-sized industrial and service companies headquartered in Brazil. A quantitative analysis was performed, and both the reliability and validity of the scales were evaluated prior to using structural equation modeling. The results demonstrate that the direct effects among BPO, analytical indicators and performance can be taken as statistically significant. The findings also demonstrate that BPO and analytical indicators can be taken as predictors of performance. The paper discusses these results and their managerial implications, as well as some research paths for future studies on the topic.
Minibrain and Wings apart control organ growth and tissue patterning through down-regulation of Capicua

Significance The transcriptional repressor protein Capicua (Cic) is a conserved regulator of organ growth and tissue patterning, and mutations in the CIC gene in humans result in the brain cancer oligodendroglioma. Cic activity is controlled by the receptor tyrosine kinase (RTK) signaling pathway. Here, we identify the kinase Minibrain (Mnb) and its adaptor Wings apart (Wap) as Cic regulators. Mnb and Wap bind to and phosphorylate the Cic protein, and inhibit the ability of Cic to repress gene expression. Mnb-dependent down-regulation of Cic is necessary for the proper growth of multiple organs and correct the patterning of tissues. Our results uncover a previously unknown mechanism of Cic regulation that acts in parallel to other growth-controlling pathways. The transcriptional repressor Capicua (Cic) controls tissue patterning and restricts organ growth, and has been recently implicated in several cancers. Cic has emerged as a primary sensor of signaling downstream of the receptor tyrosine kinase (RTK)/extracellular signal-regulated kinase (ERK) pathway, but how Cic activity is regulated in different cellular contexts remains poorly understood. We found that the kinase Minibrain (Mnb, ortholog of mammalian DYRK1A), acting through the adaptor protein Wings apart (Wap), physically interacts with and phosphorylates the Cic protein. Mnb and Wap inhibit Cic function by limiting its transcriptional repressor activity. Down-regulation of Cic by Mnb/Wap is necessary for promoting the growth of multiple organs, including the wings, eyes, and the brain, and for proper tissue patterning in the wing. We have thus uncovered a previously unknown mechanism of down-regulation of Cic activity by Mnb and Wap, which operates independently from the ERK-mediated control of Cic. Therefore, Cic functions as an integrator of upstream signals that are essential for tissue patterning and organ growth. Finally, because DYRK1A and CIC exhibit, respectively, prooncogenic vs. tumor suppressor activities in human oligodendroglioma, our results raise the possibility that DYRK1A may also down-regulate CIC in human cells.
Perplexing cooperative folding and stability of a low-sequence complexity, polyproline 2 protein lacking a hydrophobic core

Significance The basis of protein-folding cooperativity and stability elicits a variety of opinions, as does the existence and importance of possible residual structure in the denatured state. We examine these issues in a protein that is striking in its dearth of hydrophobic burial and its lack of canonical α and β structures, while having a low sequence complexity with 46% glycine. Unexpectedly, the protein’s folding behavior is similar to that observed for typical globular proteins. This enigma forces a reexamination of the possible combination of factors that can stabilize a protein. The burial of hydrophobic side chains in a protein core generally is thought to be the major ingredient for stable, cooperative folding. Here, we show that, for the snow flea antifreeze protein (sfAFP), stability and cooperativity can occur without a hydrophobic core, and without α-helices or β-sheets. sfAFP has low sequence complexity with 46% glycine and an interior filled only with backbone H-bonds between six polyproline 2 (PP2) helices. However, the protein folds in a kinetically two-state manner and is moderately stable at room temperature. We believe that a major part of the stability arises from the unusual match between residue-level PP2 dihedral angle bias in the unfolded state and PP2 helical structure in the native state. Additional stabilizing factors that compensate for the dearth of hydrophobic burial include shorter and stronger H-bonds, and increased entropy in the folded state. These results extend our understanding of the origins of cooperativity and stability in protein folding, including the balance between solvent and polypeptide chain entropies.
No growth stimulation of Canada’s boreal forest under half-century of combined warming and CO2 fertilization

Significance Limited knowledge about the mechanistic drivers of forest growth and responses to environmental changes creates uncertainties about the future role of circumpolar boreal forests in the global carbon cycle. Here, we use newly acquired tree-ring data from Canada’s National Forest Inventory to determine the growth response of the boreal forest to environmental changes. We find no consistent boreal-wide growth response over the past 60 y across Canada. However, some southwestern and southeastern forests experienced a growth enhancement, and some regions such as the northwestern and maritime areas experienced a growth depression. Growth–climate relationships bring evidence of an intensification of the impacts of hydroclimatic variability on growth late in the 20th century, in parallel with the rapid rise of summer temperature. Considerable evidence exists that current global temperatures are higher than at any time during the past millennium. However, the long-term impacts of rising temperatures and associated shifts in the hydrological cycle on the productivity of ecosystems remain poorly understood for mid to high northern latitudes. Here, we quantify species-specific spatiotemporal variability in terrestrial aboveground biomass stem growth across Canada’s boreal forests from 1950 to the present. We use 873 newly developed tree-ring chronologies from Canada’s National Forest Inventory, representing an unprecedented degree of sampling standardization for a large-scale dendrochronological study. We find significant regional- and species-related trends in growth, but the positive and negative trends compensate each other to yield no strong overall trend in forest growth when averaged across the Canadian boreal forest. The spatial patterns of growth trends identified in our analysis were to some extent coherent with trends estimated by remote sensing, but there are wide areas where remote-sensing information did not match the forest growth trends. Quantifications of tree growth variability as a function of climate factors and atmospheric CO2 concentration reveal strong negative temperature and positive moisture controls on spatial patterns of tree growth rates, emphasizing the ecological sensitivity to regime shifts in the hydrological cycle. An enhanced dependence of forest growth on soil moisture during the late-20th century coincides with a rapid rise in summer temperatures and occurs despite potential compensating effects from increased atmospheric CO2 concentration.
β-Catenin haploinsufficiency promotes mammary tumorigenesis in an ErbB2-positive basal breast cancer model

Significance Although the oncogenic potential of β-catenin as a transcriptional factor is well-established, its role as a critical component of adherens junctions during tumorigenesis remains elusive. Using two transgenic mouse models of ErbB2-induced mammary tumorigenesis that recapitulate either luminal or basal human breast cancer, we show that β-catenin is required for proper adherens junction formation and that, consequently, β-catenin haploinsufficiency promotes aggressive mammary tumorigenesis. This haploinsufficient phenotype is unique to a basal ErbB2-driven model with a preexisting aberrant activation of β-catenin signaling, highlighting a tumor suppressor role of β-catenin, similar to other adherens junction proteins, in maintaining junctional integrity and a complex interplay between its junctional and transcriptional roles in facilitating tumor progression. Aberrant activation of β-catenin through its activity as a transcription factor has been observed in a large proportion of human malignancies. Despite the improved understanding of the β-catenin signaling pathway over the past three decades, attempts to develop therapies targeting β-catenin remain challenging, and none of these targeted therapies have advanced to the clinic. In this study, we show that part of the challenge in antagonizing β-catenin is caused by its dual functionality as a cell adhesion molecule and a signaling molecule. In a mouse model of basal ErbB2 receptor tyrosine kinase 2 (ErbB2)-positive breast cancer (ErbB2KI), which exhibits aberrant β-catenin nuclear signaling, β-catenin haploinsufficiency induced aggressive tumor formation and metastasis by promoting the disruption of adherens junctions, dedifferentiation, and an epithelial to mesenchymal transition (EMT) transcriptional program. In contrast to the accelerated tumor onset observed in the haploid-insufficient ErbB2 tumors, deletion of both β-catenin alleles in the ErbB2KI model had only a minor impact on tumor onset that further correlated with the retention of normal adherens junctions. We further showed that retention of adherens junctional integrity was caused by the up-regulation of the closely related family member plakoglobin (γ-catenin) that maintained both adherens junctions and the activation of Wnt target genes. In contrast to the ErbB2KI basal tumor model, modulation of β-catenin levels had no appreciable impact on tumor onset in an ErbB2-driven model of luminal breast cancer [murine mammary tumor virus promoter (MMTV-NIC)]. These observations argue that the balance of junctional and nuclear β-catenin activity has a profound impact on tumor progression in this basal model of ErbB2-positive breast cancer.
Highly Efficient Perovskite–Perovskite Tandem Solar Cells Reaching 80% of the Theoretical Limit in Photovoltage

Organic–inorganic hybrid perovskite multijunction solar cells have immense potential to realize power conversion efficiencies (PCEs) beyond the Shockley–Queisser limit of single‐junction solar cells; however, they are limited by large nonideal photovoltage loss (V oc,loss) in small‐ and large‐bandgap subcells. Here, an integrated approach is utilized to improve the V oc of subcells with optimized bandgaps and fabricate perovskite–perovskite tandem solar cells with small V oc,loss. A fullerene variant, Indene‐C60 bis‐adduct, is used to achieve optimized interfacial contact in a small‐bandgap (≈1.2 eV) subcell, which facilitates higher quasi‐Fermi level splitting, reduces nonradiative recombination, alleviates hysteresis instabilities, and improves V oc to 0.84 V. Compositional engineering of large‐bandgap (≈1.8 eV) perovskite is employed to realize a subcell with a transparent top electrode and photostabilized V oc of 1.22 V. The resultant monolithic perovskite–perovskite tandem solar cell shows a high V oc of 1.98 V (approaching 80% of the theoretical limit) and a stabilized PCE of 18.5%. The significantly minimized nonideal V oc,loss is better than state‐of‐the‐art silicon–perovskite tandem solar cells, which highlights the prospects of using perovskite–perovskite tandems for solar‐energy generation. It also unlocks opportunities for solar water splitting using hybrid perovskites with solar‐to‐hydrogen efficiencies beyond 15%.