bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Serpukhovian–Bashkirian Amalgamation of Laurussia and the Siberian Continent and Implications for Assembly of Pangea
Authors: Xu Yan , Han Bao‐Fu , Liao Wen , Li Ang 
Published: March 2022

AbstractThe final assembly of Pangea is thought to be marked by the Siberia‐Laurussia amalgamation during the Late Carboniferous–Permian, but there are large uncertainties on the timing of the amalgamation in the previous paleogeographic reconstructions because there are no high‐quality Carboniferous–Permian paleomagnetic data available from the Siberian continent. The Zharma‐Saur area in the junction between the Siberia‐Laurussia amalgamation, involving the Zharma‐Saur arc on the northern margin of the Kazakhstan microcontinent, the South Chinese Altai terrane in the southern margin of the Siberian continent and the Irtysh‐Zaisan suture in between, can provide crucial geological constraints for the assembly of Pangea. In the Zharma‐Saur arc, the Tournaisian–Visean marine sequences are interbedded with thick pillow lavas, which were formed during southward subduction of the Irtysh‐Zaisan Ocean and unconformably covered by the Moscovian terrestrial bimodal volcanic associations and sedimentary successions, in which the basalts are columnar‐jointed in structure and the sandstones also contain the detritus derived from the South Chinese Altai terrane. The Serpukhovian–Bashkirian unconformity was coeval with the transition from the Tournaisian–Visean calc‐alkaline to the Moscovian–Early Permian high alkaline and bimodal volcanism. These dramatic changes in sedimentary environments, provenances and volcanism together indicate the Siberia‐Laurussia amalgamation during the Serpukhovian–Bashkirian and this event was almost simultaneous with the Laurussia‐Gondwana collision and the welding of Laurussia with the Kazakhstan microcontinent, but slightly earlier than the Laurussia‐Tarim collision. Therefore, the final assembly of Pangea could be completed in the Late Carboniferous.
Raindrop energy-powered autonomous wireless hyetometer based on liquid–solid contact electrification
Authors: Xu Chaoqun , Fu Xianpeng , Li Chengyu , Liu Guoxu , Gao Yuyu , Qi Youchao , Bu Tianzhao , Chen Yuanfen , Wang Zhong Lin , Zhang Chi 
Published: March 2022

AbstractTriboelectric nanogenerators (TENGs) can directly harvest energy via solid–liquid interface contact electrification, making them very suitable for harvesting raindrop energy and as active rainfall sensors. This technology is promising for realizing a fully self-powered system for autonomous rainfall monitoring combined with energy harvesting/sensing. Here, we report a raindrop energy-powered autonomous rainfall monitoring and wireless transmission system (R-RMS), in which a raindrop-TENG (R-TENG) array simultaneously serves as a raindrop energy harvester and rainfall sensor. At a rainfall intensity of 71 mm/min, the R-TENG array can generate an average short-circuit current, open-circuit voltage, and maximum output power of 15 μA, 1800 V, and 325 μW, respectively. The collected energy can be adjusted to act as a stable 2.5 V direct-current source for the whole system by a power management circuit. Meanwhile, the R-TENG array acts as a rainfall sensor, in which the output signal can be monitored and the measured data are wirelessly transmitted. Under a rainfall intensity of 71 mm/min, the R-RMS can be continuously powered and autonomously transmit rainfall data once every 4 min. This work has paved the way for raindrop energy-powered wireless hyetometers, which have exhibited broad prospects in unattended weather monitoring, field surveys, and the Internet of Things.
Cognitive glucose sensitivity—proposing a link between cognitive performance and reliance on external glucose uptake
Authors: Neukirchen Tobias , Radach Ralph , Vorstius Christian 
Published: March 2022

AbstractExisting evidence on the effects of glucose supplementation on cognitive performance appears inconclusive. Metabolic switching offers an approach to explain such incoherent findings based on differences in cognitive functioning after fasting. We propose a new construct, cognitive glucose sensitivity (CGS), which quantifies individual performance gain due to glucose supplementation. We tested the hypothesis that the effects of glucose ingestion depend on CGS, cognitive task domain, and sex. In addition, the relationship between CGS and body mass index (BMI) was examined. Seventy-one participants (48 female) were tested in two conditions each (deprivation baseline vs. glucose supplementation), performing tasks from different cognitive domains (memory and executive functioning). We found significant evidence for a correlation of deprivation baseline performance and CGS across domains (Corsi-Block-Tapping Task: r = −0.57, p < 0.001; Go-No-Go Task: r = 0.39, p = 0.001; word list recall: r = −0.50, p < 0.001). Moreover, individual CGS differed significantly between tasks (p = 0.018). Only in men, BMI was significantly related to CGS in a word recall paradigm (r = 0.49, p = 0.017). Our findings support the notion that the effects of glucose depend on CGS, task domain, and sex. The effort to reduce performance impairment (short-term) might sacrifice independence from external glucose (long term), possibly via declining blood glucose regulation. Therefore, CGS could be regarded as a candidate to enhance our understanding of the etiology of unhealthy eating.
Clinical utility of combinatorial pharmacogenomic testing in depression: A Canadian patient- and rater-blinded, randomized, controlled trial
Authors: Tiwari Arun K. , Zai Clement C. , Altar C. Anthony , Tanner Julie-Anne , Davies Paige E. , Traxler Paul , Li James , Cogan Elizabeth S. , Kucera Matthew T. , Gugila Ana , Braganza Nicole , Emmerson Heather , Zai Gwyneth , Müller Daniel J. , Levitan Robert , Kloiber Stefan , Daskalakis Zafiris J. , Frey Benicio N. , Bowen James M. , Tarride Jean-Eric , Tytus Richard , Chandrasena Ranjith , Voudouris Nicholas , Taylor Valerie H. , Tempier Raymond , Sharma Verinder , Vasudev Akshya , Dzongowski Peter , Pliamm Lew , Greenspoon Todd , Dechairo Bryan M. , Kennedy James L. 
Published: March 2022

AbstractThe pharmacological treatment of depression consists of stages of trial and error, with less than 40% of patients achieving remission during first medication trial. However, in a large, randomized-controlled trial (RCT) in the U.S. (“GUIDED”), significant improvements in response and remission rates were observed in patients who received treatment guided by combinatorial pharmacogenomic testing, compared to treatment-as-usual (TAU). Here we present results from the Canadian “GAPP-MDD” RCT. This 52-week, 3-arm, multi-center, participant- and rater-blinded RCT evaluated clinical outcomes among patients with depression whose treatment was guided by combinatorial pharmacogenomic testing compared to TAU. The primary outcome was symptom improvement (change in 17-item Hamilton Depression Rating Scale, HAM-D17) at week 8. Secondary outcomes included response (≥50% decrease in HAM-D17) and remission (HAM-D17 ≤ 7) at week 8. Numerically, patients in the guided-care arm had greater symptom improvement (27.6% versus 22.7%), response (30.3% versus 22.7%), and remission rates (15.7% versus 8.3%) compared to TAU, although these differences were not statistically significant. Given that the GAPP-MDD trial was ultimately underpowered to detect statistically significant differences in patient outcomes, it was assessed in parallel with the larger GUIDED RCT. We observed that relative improvements in response and remission rates were consistent between the GAPP-MDD (33.0% response, 89.0% remission) and GUIDED (31.0% response, 51.0% remission) trials. Together with GUIDED, the results from the GAPP-MDD trial indicate that combinatorial pharmacogenomic testing can be an effective tool to help guide depression treatment in the context of the Canadian healthcare setting (ClinicalTrials.gov NCT02466477).
Distinct contributions of GluA1-containing AMPA receptors of different hippocampal subfields to salience processing, memory and impulse control
Authors: Kilonzo Kasyoka , Strahnen Daniel , Prex Vivien , Gems John , van der Veen Bastiaan , Kapanaiah Sampath K. T. , Murthy Bhargavi K. B. , Schulz Stefanie , Sprengel Rolf , Bannerman David , Kätzel Dennis 
Published: March 2022

AbstractSchizophrenia is associated with a broad range of severe and currently pharmacoresistant cognitive deficits. Prior evidence suggests that hypofunction of AMPA-type glutamate receptors (AMPARs) containing the subunit GLUA1, encoded by GRIA1, might be causally related to impairments of selective attention and memory in this disorder, at least in some patients. In order to clarify the roles of GluA1 in distinct cell populations, we investigated behavioural consequences of selective Gria1-knockout in excitatory neurons of subdivisions of the prefrontal cortex and the hippocampus, assessing sustained attention, impulsivity, cognitive flexibility, anxiety, sociability, hyperactivity, and various forms of short-term memory in mice. We found that virally induced reduction of GluA1 across multiple hippocampal subfields impaired spatial working memory. Transgene-mediated ablation of GluA1 from excitatory cells of CA2 impaired short-term memory for conspecifics and objects. Gria1 knockout in CA3 pyramidal cells caused mild impairments of object-related and spatial short-term memory, but appeared to partially increase social interaction and sustained attention and to reduce motor impulsivity. Our data suggest that reduced hippocampal GluA1 expression—as seen in some patients with schizophrenia—may be a central cause particularly for several short-term memory deficits. However, as impulse control and sustained attention actually appeared to improve with GluA1 ablation in CA3, strategies of enhancement of AMPAR signalling likely require a fine balance to be therapeutically effective across the broad symptom spectrum of schizophrenia.
Rubicon-deficiency sensitizes mice to mixed lineage kinase domain-like (MLKL)-mediated kidney ischemia-reperfusion injury
Authors: Tonnus Wulf , Locke Sophie , Meyer Claudia , Maremonti Francesca , Eggert Lena , von Mässenhausen Anne , Bornstein Stefan R. , Green Douglas R. , Linkermann Andreas 
Published: March 2022

AbstractThe cytosolic protein rubicon (RUBCN) has been implicated in the removal of necrotic debris and autoimmunity. However, the role of RUBCN in models of acute kidney injury (AKI), a condition that typically involves necrotic kidney tubules, was not investigated. Here, we demonstrate that RUBCN-deficient mice are hypersensitive to renal damage induced by ischemia-reperfusion injury (IRI) and cisplatin-induced AKI. Combined deficiency of RUBCN and mixed lineage kinase domain-like (MLKL) partially reversed the sensitivity in the IRI model suggesting that the absence of RUBCN sensitizes to necroptosis in that model. Necroptosis is known to contribute to TNFα-induced severe inflammatory response syndrome (SIRS), but we detected no statistically significant difference in overall survival following injection of TNFα in RUBCN-deficient mice. We additionally generated RUBCN-deficient mice which lack gasdermin D (GSDMD), the terminal mediator of pyroptosis, but no reversal of the AKI phenotype was observed. Finally, and in contrast to the previous understanding of the role of RUBCN, we did not find a significant autoimmune phenotype in RUBCN-deficient mice, but detected chronic kidney injury (CKD) in aged RUBCN-deficient mice of both sexes. In summary, our data indicate that RUBCN-deficient mice are hypersensitive to kidney injury.
An integrated bioinformatic investigation of mitochondrial solute carrier family 25 (SLC25) in colon cancer followed by preliminary validation of member 5 (SLC25A5) in tumorigenesis
Authors: Chen Yan-Jie , Hong Wei-Feng , Liu Meng-Ling , Guo Xi , Yu Yi-Yi , Cui Yue-Hong , Liu Tian-Shu , Liang Li 
Published: March 2022

AbstractSolute carrier family 25 (SLC25) encodes transport proteins at the inner mitochondrial membrane and functions as carriers for metabolites. Although SLC25 genetic variants correlate with human metabolic diseases, their roles in colon cancer remain unknown. Cases of colon cancer were retrieved from The Cancer Genome Atlas, and the transcriptionally differentially expressed members (DEMs) of SLC25 were identified. DNA level alterations, clinicopathological characteristics, and clinical survival were also investigated. A risk score model based on the DEMs was constructed to further evaluate their prognostic values in a clinical setting. The results were preliminarily validated using bioinformatic analysis of datasets from the Gene Expression Omnibus, immunohistochemical evaluations in clinical specimens, and functional experiments in colon cancer-derived cell lines. Thirty-seven DEMs were identified among 53 members of SLC25. Eight of 37 DEMs were introduced into a risk score model using integrated LASSO regression and multivariate Cox regression. Validated by GSE395282 and GSE175356, DEMs with high-risk scores were associated with the phenotypes of increasing tumor immune infiltration and decreasing glycolysis and apoptosis contents. SLC25A5 was downregulated in cancer, and its upregulation was related to better overall survival in patients from public datasets and in clinical cases. High SLC25A5 expression was an independent prognostic factor for 79 patients after surgical treatment. A negative correlation between CD8 and SLC25A5 was determined in specimens from 106 patients with advanced colon cancer. SLC25A5 attenuated cell proliferation, upregulated the expression of programmed cell death-related signatures, and exerted its biological function by inhibiting the MAPK signaling pathway. Our study reveals that mitochondrial SLC25 has prognostic value in patients with colon cancer. The bioinformatic analyses by following verification in situ and in vitro provide direction for further functional and mechanistic studies on the identified member of SLC25.
Hyperglycemia-triggered ATF6-CHOP pathway aggravates acute inflammatory liver injury by β-catenin signaling
Authors: Yang Chao , Wang Zeng , Hu Yuanchang , Yang Shikun , Cheng Feng , Rao Jianhua , Wang Xuehao 
Published: March 2022

AbstractAlthough hyperglycemia has been documented as an unfavorable element that can further induce liver ischemia–reperfusion injury (IRI), the related molecular mechanisms remain to be clearly elaborated. This study investigated the effective manner of endoplasmic reticulum (ER) stress signaling in hyperglycemia-exacerbated liver IRI. Here we demonstrated that in the liver tissues and Kupffer cells (KCs) of DM patients and STZ-induced hyperglycemic mice, the ER stress-ATF6-CHOP signaling pathway is activated. TLR4-mediated pro-inflammatory activation was greatly attenuated by the addition of 4-phenylbutyrate (PBA), one common ER stress inhibitor. The liver IRI in hyperglycemic mice was also significantly reduced after PBA treatment. In addition, deficiency of CHOP (CHOP−/−) obviously alleviates the hepatic IRI, and pro-inflammatory effects deteriorated by hyperglycemia. In hyperglycemic mice, β-catenin expression was suppressed while the ATF6-CHOP signal was activated. In the liver tissues of PBA-treated or CHOP−/− hyperglycemic mice, the expression of β-catenin was restored. Furthermore, CHOP deficiency can induce protection against hyperglycemia-related liver IRI, which was disrupted by the knockdown of β-catenin will cause this protection to disappear. High glucose (HG) treatment stimulated ATF6-CHOP signaling, reduced cellular β-catenin accumulation, and promoted the TLR4-related inflammation of BMDMs. But the above effects were partially rescued in BMDMs with CHOP deficiency or by PBA treatment. In BMDMs cultured in HG conditions, the anti-inflammatory functions of CHOP−/− were destroyed by the knockdown of β-catenin. Finally, chimeric mice carrying WT or CHOP−/− BMDMs by bone marrow transplantation were adopted to verify the above conclusion. The current study suggested that hyperglycemia could trigger ER stress-ATF6-CHOP axis, inhibit β-catenin activation, accelerate inflammation, and deteriorate liver IRI, thus providing the treatment potential for management of sterile liver inflammation in DM patients.
A specialized bone marrow microenvironment for fetal haematopoiesis
Authors: Liu Yang , Chen Qi , Jeong Hyun-Woo , Koh Bong Ihn , Watson Emma C. , Xu Cong , Stehling Martin , Zhou Bin , Adams Ralf H. 
Published: March 2022

AbstractIn adult mammalian bone marrow (BM), vascular endothelial cells and perivascular reticular cells control the function of haematopoietic stem and progenitor cells (HSPCs). During fetal development, the mechanisms regulating the de novo haematopoietic cell colonization of BM remain largely unknown. Here, we show that fetal and adult BM exhibit fundamental differences in cellular composition and molecular interactions by single cell RNA sequencing. While fetal femur is largely devoid of leptin receptor-expressing cells, arterial endothelial cells (AECs) provide Wnt ligand to control the initial HSPC expansion. Haematopoietic stem cells and c-Kit+ HSPCs are reduced when Wnt secretion by AECs is genetically blocked. We identify Wnt2 as AEC-derived signal that activates β-catenin-dependent proliferation of fetal HSPCs. Treatment of HSPCs with Wnt2 promotes their proliferation and improves engraftment after transplantation. Our work reveals a fundamental switch in the cellular organization and molecular regulation of BM niches in the embryonic and adult organism.
Texture is encoded in precise temporal spiking patterns in primate somatosensory cortex
Authors: Long Katie H. , Lieber Justin D. , Bensmaia Sliman J. 
Published: March 2022

AbstractHumans are exquisitely sensitive to the microstructure and material properties of surfaces. In the peripheral nerves, texture information is conveyed via two mechanisms: coarse textural features are encoded in spatial patterns of activation that reflect their spatial layout, and fine features are encoded in highly repeatable, texture-specific temporal spiking patterns evoked as the skin moves across the surface. Here, we examined whether this temporal code is preserved in the responses of neurons in somatosensory cortex. We scanned a diverse set of everyday textures across the fingertip of awake macaques while recording the responses evoked in individual cortical neurons. We found that temporal spiking patterns are highly repeatable across multiple presentations of the same texture, with millisecond precision. As a result, texture identity can be reliably decoded from the temporal patterns themselves, even after information carried in the spike rates is eliminated. However, the combination of rate and timing is more informative than either code in isolation. The temporal precision of the texture response is heterogenous across cortical neurons and depends on the submodality composition of their input and on their location along the somatosensory neuraxis. Furthermore, temporal spiking patterns in cortex dilate and contract with decreases and increases in scanning speed, respectively, and this systematic relationship between speed and patterning may contribute to the observed perceptual invariance to speed. Finally, we find that the quality of a texture percept can be better predicted when these temporal patterns are taken into consideration. We conclude that high-precision spike timing complements rate-based signals to encode texture in somatosensory cortex.
Lysosomal Ca2+-mediated TFEB activation modulates mitophagy and functional adaptation of pancreatic β-cells to metabolic stress
Authors: Park Kihyoun , Lim Hyejin , Kim Jinyoung , Hwang Yeseong , Lee Yu Seol , Bae Soo Han , Kim Hyeongseok , Kim Hail , Kang Shin-Wook , Kim Joo Young , Lee Myung-Shik 
Published: March 2022

AbstractAlthough autophagy is critical for pancreatic β-cell function, the role and mechanism of mitophagy in β-cells are unclear. We studied the role of lysosomal Ca2+ in TFEB activation by mitochondrial or metabolic stress and that of TFEB-mediated mitophagy in β-cell function. Mitochondrial or metabolic stress induced mitophagy through lysosomal Ca2+ release, increased cytosolic Ca2+ and TFEB activation. Lysosomal Ca2+ replenishment by ER- > lysosome Ca2+ refilling was essential for mitophagy. β-cell-specific Tfeb knockout (TfebΔβ-cell) abrogated high-fat diet (HFD)-induced mitophagy, accompanied by increased ROS and reduced mitochondrial cytochrome c oxidase activity or O2 consumption. TfebΔβ-cell mice showed aggravation of HFD-induced glucose intolerance and impaired insulin release. Metabolic or mitochondrial stress induced TFEB-dependent expression of mitophagy receptors including Ndp52 and Optn, contributing to the increased mitophagy. These results suggest crucial roles of lysosomal Ca2+ release coupled with ER- > lysosome Ca2+ refilling and TFEB activation in mitophagy and maintenance of pancreatic β-cell function during metabolic stress.
An achromatic X-ray lens
Authors: Kubec Adam , Zdora Marie-Christine , Sanli Umut T. , Diaz Ana , Vila-Comamala Joan , David Christian 
Published: March 2022

AbstractDiffractive and refractive optical elements have become an integral part of most high-resolution X-ray microscopes. However, they suffer from inherent chromatic aberration. This has to date restricted their use to narrow-bandwidth radiation, essentially limiting such high-resolution X-ray microscopes to high-brightness synchrotron sources. Similar to visible light optics, one way to tackle chromatic aberration is by combining a focusing and a defocusing optic with different dispersive powers. Here, we present the first successful experimental realisation of an X-ray achromat, consisting of a focusing diffractive Fresnel zone plate (FZP) and a defocusing refractive lens (RL). Using scanning transmission X-ray microscopy (STXM) and ptychography, we demonstrate sub-micrometre achromatic focusing over a wide energy range without any focal adjustment. This type of X-ray achromat will overcome previous limitations set by the chromatic aberration of diffractive and refractive optics and paves the way for new applications in spectroscopy and microscopy at broadband X-ray tube sources.
Phylogenomic analyses highlight innovation and introgression in the continental radiations of Fagaceae across the Northern Hemisphere
Authors: Zhou Biao-Feng , Yuan Shuai , Crowl Andrew A. , Liang Yi-Ye , Shi Yong , Chen Xue-Yan , An Qing-Qing , Kang Ming , Manos Paul S. , Wang Baosheng 
Published: March 2022

AbstractNorthern Hemisphere forests changed drastically in the early Eocene with the diversification of the oak family (Fagaceae). Cooling climates over the next 20 million years fostered the spread of temperate biomes that became increasingly dominated by oaks and their chestnut relatives. Here we use phylogenomic analyses of nuclear and plastid genomes to investigate the timing and pattern of major macroevolutionary events and ancient genome-wide signatures of hybridization across Fagaceae. Innovation related to seed dispersal is implicated in triggering waves of continental radiations beginning with the rapid diversification of major lineages and resulting in unparalleled transformation of forest dynamics within 15 million years following the K-Pg extinction. We detect introgression at multiple time scales, including ancient events predating the origination of genus-level diversity. As oak lineages moved into newly available temperate habitats in the early Miocene, secondary contact between previously isolated species occurred. This resulted in adaptive introgression, which may have further amplified the diversification of white oaks across Eurasia.