bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nanosecond-resolution photothermal dynamic imaging via MHZ digitization and match filtering
Authors: Yin Jiaze , Lan Lu , Zhang Yi , Ni Hongli , Tan Yuying , Zhang Meng , Bai Yeran , Cheng Ji-Xin 
Published: December 2021

AbstractPhotothermal microscopy has enabled highly sensitive label-free imaging of absorbers, from metallic nanoparticles to chemical bonds. Photothermal signals are conventionally detected via modulation of excitation beam and demodulation of probe beam using lock-in amplifier. While convenient, the wealth of thermal dynamics is not revealed. Here, we present a lock-in free, mid-infrared photothermal dynamic imaging (PDI) system by MHz digitization and match filtering at harmonics of modulation frequency. Thermal-dynamic information is acquired at nanosecond resolution within single pulse excitation. Our method not only increases the imaging speed by two orders of magnitude but also obtains four-fold enhancement of signal-to-noise ratio over lock-in counterpart, enabling high-throughput metabolism analysis at single-cell level. Moreover, by harnessing the thermal decay difference between water and biomolecules, water background is effectively separated in mid-infrared PDI of living cells. This ability to nondestructively probe chemically specific photothermal dynamics offers a valuable tool to characterize biological and material specimens.
Plasmin activity promotes amyloid deposition in a transgenic model of human transthyretin amyloidosis
Authors: Slamova Ivana , Adib Rozita , Ellmerich Stephan , Golos Michal R. , Gilbertson Janet A. , Botcher Nicola , Canetti Diana , Taylor Graham W. , Rendell Nigel , Tennent Glenys A. , Verona Guglielmo , Porcari Riccardo , Mangione P. Patrizia , Gillmore Julian D. , Pepys Mark B. , Bellotti Vittorio , Hawkins Philip N. , Al-Shawi Raya , Simons J. Paul 
Published: December 2021

AbstractCardiac ATTR amyloidosis, a serious but much under-diagnosed form of cardiomyopathy, is caused by deposition of amyloid fibrils derived from the plasma protein transthyretin (TTR), but its pathogenesis is poorly understood and informative in vivo models have proved elusive. Here we report the generation of a mouse model of cardiac ATTR amyloidosis with transgenic expression of human TTRS52P. The model is characterised by substantial ATTR amyloid deposits in the heart and tongue. The amyloid fibrils contain both full-length human TTR protomers and the residue 49-127 cleavage fragment which are present in ATTR amyloidosis patients. Urokinase-type plasminogen activator (uPA) and plasmin are abundant within the cardiac and lingual amyloid deposits, which contain marked serine protease activity; knockout of α2-antiplasmin, the physiological inhibitor of plasmin, enhances amyloid formation. Together, these findings indicate that cardiac ATTR amyloid deposition involves local uPA-mediated generation of plasmin and cleavage of TTR, consistent with the previously described mechano-enzymatic hypothesis for cardiac ATTR amyloid formation. This experimental model of ATTR cardiomyopathy has potential to allow further investigations of the factors that influence human ATTR amyloid deposition and the development of new treatments.
An injury-induced serotonergic neuron subpopulation contributes to axon regrowth and function restoration after spinal cord injury in zebrafish
Authors: Huang Chun-Xiao , Zhao Yacong , Mao Jie , Wang Zhen , Xu Lulu , Cheng Jianwei , Guan Na N. , Song Jianren 
Published: December 2021

AbstractSpinal cord injury (SCI) interrupts long-projecting descending spinal neurons and disrupts the spinal central pattern generator (CPG) that controls locomotion. The intrinsic mechanisms underlying re-wiring of spinal neural circuits and recovery of locomotion after SCI are unclear. Zebrafish shows axonal regeneration and functional recovery after SCI making it a robust model to study mechanisms of regeneration. Here, we use a two-cut SCI model to investigate whether recovery of locomotion can occur independently of supraspinal connections. Using this injury model, we show that injury induces the localization of a specialized group of intraspinal serotonergic neurons (ISNs), with distinctive molecular and cellular properties, at the injury site. This subpopulation of ISNs have hyperactive terminal varicosities constantly releasing serotonin activating 5-HT1B receptors, resulting in axonal regrowth of spinal interneurons. Axon regrowth of excitatory interneurons is more pronounced compared to inhibitory interneurons. Knock-out of htr1b prevents axon regrowth of spinal excitatory interneurons, negatively affecting coordination of rostral-caudal body movements and restoration of locomotor function. On the other hand, treatment with 5-HT1B receptor agonizts promotes functional recovery following SCI. In summary, our data show an intraspinal mechanism where a subpopulation of ISNs stimulates axonal regrowth resulting in improved recovery of locomotor functions following SCI in zebrafish.
Oxidative stress-induced FABP5 S-glutathionylation protects against acute lung injury by suppressing inflammation in macrophages
Authors: Guo Yuxian , Liu Yaru , Zhao Shihao , Xu Wangting , Li Yiqing , Zhao Pengwei , Wang Di , Cheng Hongqiang , Ke Yuehai , Zhang Xue 
Published: December 2021

AbstractOxidative stress contributes to the pathogenesis of acute lung injury. Protein S-glutathionylation plays an important role in cellular antioxidant defense. Here we report that the expression of deglutathionylation enzyme Grx1 is decreased in the lungs of acute lung injury mice. The acute lung injury induced by hyperoxia or LPS is significantly relieved in Grx1 KO and Grx1fl/flLysMcremice, confirming the protective role of Grx1-regulated S-glutathionylation in macrophages. Using a quantitative redox proteomics approach, we show that FABP5 is susceptible to S-glutathionylation under oxidative conditions. S-glutathionylation of Cys127 in FABP5 promotes its fatty acid binding ability and nuclear translocation. Further results indicate S-glutathionylation promotes the interaction of FABP5 and PPARβ/δ, activates PPARβ/δ target genes and suppresses the LPS-induced inflammation in macrophages. Our study reveals a molecular mechanism through which FABP5 S-glutathionylation regulates macrophage inflammation in the pathogenesis of acute lung injury.
Electric-field control of field-free spin-orbit torque switching via laterally modulated Rashba effect in Pt/Co/AlOx structures
Authors: Kang Min-Gu , Choi Jong-Guk , Jeong Jimin , Park Jae Yeol , Park Hyeon-Jong , Kim Taehwan , Lee Taekhyeon , Kim Kab-Jin , Kim Kyoung-Whan , Oh Jung Hyun , Viet Duc Duong , Jeong Jong-Ryul , Yuk Jong Min , Park Jongsun , Lee Kyung-Jin , Park Byong-Guk 
Published: December 2021

AbstractSpin-orbit coupling effect in structures with broken inversion symmetry, known as the Rashba effect, facilitates spin-orbit torques (SOTs) in heavy metal/ferromagnet/oxide structures, along with the spin Hall effect. Electric-field control of the Rashba effect is established for semiconductor interfaces, but it is challenging in structures involving metals owing to the screening effect. Here, we report that the Rashba effect in Pt/Co/AlOx structures is laterally modulated by electric voltages, generating out-of-plane SOTs. This enables field-free switching of the perpendicular magnetization and electrical control of the switching polarity. Changing the gate oxide reverses the sign of out-of-plane SOT while maintaining the same sign of voltage-controlled magnetic anisotropy, which confirms the Rashba effect at the Co/oxide interface is a key ingredient of the electric-field modulation. The electrical control of SOT switching polarity in a reversible and non-volatile manner can be utilized for programmable logic operations in spintronic logic-in-memory devices.
Observation of the ponderomotive effect in non-valence bound states of polyatomic molecular anions
Authors: Kang Do Hyung , Kim Jinwoo , Noh Heung-Ryoul , Kim Sang Kyu 
Published: December 2021

AbstractThe ponderomotive force on molecular systems has rarely been observed hitherto, despite potentially being extremely useful for the manipulation of the molecular properties. Here, the ponderomotive effect in the non-valence bound states has been experimentally demonstrated, for the first time to the best of our knowledge, giving great promise for the manipulation of polyatomic molecules by the dynamic Stark effect. Entire quantum levels of the dipole-bound state (DBS) and quadrupole-bound state (QBS) of the phenoxide (or 4-bromophenoxide) and 4-cyanophenoxide anions, respectively, show clear-cut ponderomotive blue-shifts in the presence of the spatiotemporally overlapped non-resonant picosecond control laser pulse. The quasi-free electron in the QBS is found to be more vulnerable to the external oscillating electromagnetic field compared to that in the DBS, suggesting that the non-valence orbital of the former is more diffusive and thus more polarizable compared to that of the latter.
Dynamic restructuring of supported metal nanoparticles and its implications for structure insensitive catalysis
Authors: Vogt Charlotte , Meirer Florian , Monai Matteo , Groeneveld Esther , Ferri Davide , van Santen Rutger A. , Nachtegaal Maarten , Unocic Raymond R. , Frenkel Anatoly I. , Weckhuysen Bert M. 
Published: December 2021

AbstractSome fundamental concepts of catalysis are not fully explained but are of paramount importance for the development of improved catalysts. An example is the concept of structure insensitive reactions, where surface-normalized activity does not change with catalyst metal particle size. Here we explore this concept and its relation to surface reconstruction on a set of silica-supported Ni metal nanoparticles (mean particle sizes 1–6 nm) by spectroscopically discerning a structure sensitive (CO2hydrogenation) from a structure insensitive (ethene hydrogenation) reaction. Using state-of-the-art techniques,inter aliain-situ STEM, and quick-X-ray absorption spectroscopy with sub-second time resolution, we have observed particle-size-dependent effects like restructuring which increases with increasing particle size, and faster restructuring for larger particle sizes during ethene hydrogenation while for CO2no such restructuring effects were observed. Furthermore, a degree of restructuring is irreversible, and we also show that the rate of carbon diffusion on, and into nanoparticles increases with particle size. We finally show that these particle size-dependent effects induced by ethene hydrogenation, can make a structure sensitive reaction (CO2hydrogenation), structure insensitive. We thus postulate that structure insensitive reactions are actuallyapparentlystructure insensitive, which changes our fundamental understanding of the empirical observation of structure insensitivity.
Aberrant chromatin landscape following loss of the H3.3 chaperone Daxx in haematopoietic precursors leads to Pu.1-mediated neutrophilia and inflammation
Authors: Gerber Julia P. , Russ Jenny , Chandrasekar Vijay , Offermann Nina , Lee Hang-Mao , Spear Sarah , Guzzi Nicola , Maida Simona , Pattabiraman Sundararaghavan , Zhang Ruoyu , Kayvanjoo Amir H. , Datta Preeta , Kasturiarachchi Jagath , Sposito Teresa , Izotova Natalia , Händler Kristian , Adams Peter D. , Marafioti Teresa , Enver Tariq , Wenzel Jörg , Beyer Marc , Mass Elvira , Bellodi Cristian , Schultze Joachim L. , Capasso Melania , Nimmo Rachael , Salomoni Paolo 
Published: December 2021

AbstractDefective silencing of retrotransposable elements has been linked to inflammageing, cancer and autoimmune diseases. However, the underlying mechanisms are only partially understood. Here we implicate the histone H3.3 chaperone Daxx, a retrotransposable element repressor inactivated in myeloid leukaemia and other neoplasms, in protection from inflammatory disease. Loss of Daxx alters the chromatin landscape, H3.3 distribution and histone marks of haematopoietic progenitors, leading to engagement of a Pu.1-dependent transcriptional programme for myelopoiesis at the expense of B-cell differentiation. This causes neutrophilia and inflammation, predisposing mice to develop an autoinflammatory skin disease. While these molecular and phenotypic perturbations are in part reverted in animals lacking both Pu.1 and Daxx, haematopoietic progenitors in these mice show unique chromatin and transcriptome alterations, suggesting an interaction between these two pathways. Overall, our findings implicate retrotransposable element silencing in haematopoiesis and suggest a cross-talk between the H3.3 loading machinery and the pioneer transcription factor Pu.1.
Search for topological defect dark matter with a global network of optical magnetometers
Authors: Afach Samer , Buchler Ben C. , Budker Dmitry , Dailey Conner , Derevianko Andrei , Dumont Vincent , Figueroa Nataniel L. , Gerhardt Ilja , Grujić Zoran D. , Guo Hong , Hao Chuanpeng , Hamilton Paul S. , Hedges Morgan , Jackson Kimball Derek F. , Kim Dongok , Khamis Sami , Kornack Thomas , Lebedev Victor , Lu Zheng-Tian , Masia-Roig Hector , Monroy Madeline , Padniuk Mikhail , Palm Christopher A. , Park Sun Yool , Paul Karun V. , Penaflor Alexander , Peng Xiang , Pospelov Maxim , Preston Rayshaun , Pustelny Szymon , Scholtes Theo , Segura Perrin C. , Semertzidis Yannis K. , Sheng Dong , Shin Yun Chang , Smiga Joseph A. , Stalnaker Jason E. , Sulai Ibrahim , Tandon Dhruv , Wang Tao , Weis Antoine , Wickenbrock Arne , Wilson Tatum , Wu Teng , Wurm David , Xiao Wei , Yang Yucheng , Yu Dongrui , Zhang Jianwei 
Published: December 2021

AbstractUltralight bosons such as axion-like particles are viable candidates for dark matter. They can form stable, macroscopic field configurations in the form of topological defects that could concentrate the dark matter density into many distinct, compact spatial regions that are small compared with the Galaxy but much larger than the Earth. Here we report the results of the search for transient signals from the domain walls of axion-like particles by using the global network of optical magnetometers for exotic (GNOME) physics searches. We search the data, consisting of correlated measurements from optical atomic magnetometers located in laboratories all over the world, for patterns of signals propagating through the network consistent with domain walls. The analysis of these data from a continuous month-long operation of GNOME finds no statistically significant signals, thus placing experimental constraints on such dark matter scenarios.
Signature of long-lived memory CD8+ T cells in acute SARS-CoV-2 infection
Authors: Adamo Sarah , Michler Jan , Zurbuchen Yves , Cervia Carlo , Taeschler Patrick , Raeber Miro E. , Baghai Sain Simona , Nilsson Jakob , Moor Andreas E. , Boyman Onur 
Published: December 2021

AbstractImmunological memory is a hallmark of adaptive immunity and facilitates an accelerated and enhanced immune response upon re-infection with the same pathogen1,2. Since the outbreak of the ongoing COVID-19 pandemic, a key question has focused on which SARS-CoV-2-specific T cells stimulated during acute infection give rise to long-lived memory T cells3. Here, using spectral flow cytometry combined with cellular indexing of transcriptomes and T cell receptor sequencing, we longitudinally characterized individual SARS-CoV-2-specific CD8+ T cells of patients with COVID-19 from acute infection to 1 year into recovery and found a distinct signature identifying long-lived memory CD8+ T cells. SARS-CoV-2-specific memory CD8+ T cells persisting 1 year after acute infection express CD45RA, IL-7 receptor-α and T cell factor 1, but they maintain low expression of CCR7, thus resembling CD45RA+ effector memory T cells. Tracking individual clones of SARS-CoV-2-specific CD8+ T cells, we reveal that an interferon signature marks clones that give rise to long-lived cells, whereas prolonged proliferation and mechanistic target of rapamycin signalling are associated with clonal disappearance from the blood. Collectively, we describe a transcriptional signature that marks long-lived, circulating human memory CD8+ T cells following an acute viral infection.
An auditory-visual tradeoff in susceptibility to clutter
Authors: Zhang Min , Denison Rachel N , Pelli Denis G , Le Thuy Tien C , Ihlefeld Antje 
Published: December 2021

AbstractSensory cortical mechanisms combine auditory or visual features into perceived objects. This is difficult in noisy or cluttered environments. Knowing that individuals vary greatly in their susceptibility to clutter, we wondered whether there might be a relation between an individual’s auditory and visual susceptibilities to clutter. In auditory masking, background sound makes spoken words unrecognizable. When masking arises due to interference at central auditory processing stages, beyond the cochlea, it is called informational masking. A strikingly similar phenomenon in vision, called visual crowding, occurs when nearby clutter makes a target object unrecognizable, despite being resolved at the retina. We here compare susceptibilities to auditory informational masking and visual crowding in the same participants. Surprisingly, across participants, we find a negative correlation (R = –0.7) between susceptibility to informational masking and crowding: Participants who have low susceptibility to auditory clutter tend to have high susceptibility to visual clutter, and vice versa. This reveals a tradeoff in the brain between auditory and visual processing.
Preparation and evaluation of crocin loaded in nanoniosomes and their effects on ischemia–reperfusion injuries in rat kidney
Authors: Naderi Reyhaneh , Pardakhty Abbas , Abbasi Mohammad Farajli , Ranjbar Mehdi , Iranpour Maryam 
Published: December 2021

AbstractAs a powerful antioxidant compound, crocin can partially protect against renal ischemia/reperfusion (I/R) injuries. The encapsulation of components in niosomes (non-ionic surfactant-based vesicle) as nano-sized carrier systems has been proposed as they improve the solubility, stability, and bioavailability of drugs. Herein, the encapsulation of crocin in nano-niosomes and the effects of crocin-loaded nano-niosomes on renal ischemia/reperfusion-induced damages were evaluated. Nano-niosomes containing crocin were formulated by a modified heating method and were characterized for their physicochemical characteristics. Ischemia was induced by clamping the renal artery for 30 min followed by 1 or 24 h of reperfusion. Rats received an intra-arterial injection of nano-niosome-loaded crocin at the outset of reperfusion. Blood samples were taken after reperfusion to measure urea, creatinine (Cr), malondialdehyde (MDA), and superoxide dismutase (SOD) activity. The right kidney was removed for histological examination. The results showed that crocin-contain nano-niosomes have appropriate size and morphology, acceptable encapsulation efficiency, and a proper release pattern of crocin. I/R enhanced creatinine (Cr), urea, and malondialdehyde (MDA) serum levels and reduced SOD activity and histological damages in the renal tissue.
Ketogenic Diet as a potential treatment for traumatic brain injury in mice
Authors: Har-Even Meirav , Rubovitch Vardit , Ratliff Whitney A. , Richmond-Hacham Bar , Citron Bruce A. , Pick Chaim G. 
Published: December 2021

AbstractTraumatic brain injury (TBI) is a brain dysfunction without present treatment. Previous studies have shown that animals fed ketogenic diet (KD) perform better in learning tasks than those fed standard diet (SD) following brain injury. The goal of this study was to examine whether KD is a neuroprotective in TBI mouse model. We utilized a closed head injury model to induce TBI in mice, followed by up to 30 days of KD/SD. Elevated levels of ketone bodies were confirmed in the blood following KD. Cognitive and behavioral performance was assessed post injury and molecular and cellular changes were assessed within the temporal cortex and hippocampus. Y-maze and Novel Object Recognition tasks indicated that mTBI mice maintained on KD displayed better cognitive abilities than mTBI mice maintained on SD. Mice maintained on SD post-injury demonstrated SIRT1 reduction when compared with uninjured and KD groups. In addition, KD management attenuated mTBI-induced astrocyte reactivity in the dentate gyrus and decreased degeneration of neurons in the dentate gyrus and in the cortex. These results support accumulating evidence that KD may be an effective approach to increase the brain’s resistance to damage and suggest a potential new therapeutic strategy for treating TBI.
Butyrate producing microbiota are reduced in chronic kidney diseases
Authors: Gao Bei , Jose Adarsh , Alonzo-Palma Norma , Malik Taimur , Shankaranarayanan Divya , Regunathan-Shenk Renu , Raj Dominic S. 
Published: December 2021

AbstractChronic kidney disease is a major public health concern that affects millions of people globally. Alterations in gut microbiota composition have been observed in patients with chronic kidney disease. Nevertheless, the correlation between the gut microbiota and disease severity has not been investigated. In this study, we performed shot-gun metagenomics sequencing and identified several taxonomic and functional signatures associated with disease severity in patients with chronic kidney disease. We noted that 19 microbial genera were significantly associated with the severity of chronic kidney disease. The butyrate-producing bacteria were reduced in patients with advanced stages of chronic kidney diseases. In addition, functional metagenomics showed that two-component systems, metabolic activity and regulation of co-factor were significantly associated with the disease severity. Our study provides valuable information for the development of microbiota-oriented therapeutic strategies for chronic kidney disease.
Deregulation of ribosomal proteins in human cancers
Authors: El Khoury Wendy , Nasr Zeina 
Published: December 2021

Abstract
The ribosome, the site for protein synthesis, is composed of ribosomal RNAs (rRNAs) and ribosomal proteins (RPs). The latter have been shown to have many ribosomal and extraribosomal functions. RPs are implicated in a variety of pathological processes, especially tumorigenesis and cell transformation. In this review, we will focus on the recent advances that shed light on the effects of RPs deregulation in different types of cancer and their roles in regulating the tumor cell fate.