bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stretchable glove for accurate and robust hand pose reconstruction based on comprehensive motion data
Authors: Park Myungsun , Park Taejun , Park Soah , Yoon Sohee John , Koo Sumin Helen , Park Yong-Lae 
Published: July 2024

AbstractWe propose a compact wearable glove capable of estimating both the finger bone lengths and the joint angles of the wearer with a simple stretch-based sensing mechanism. The soft sensing glove is designed to easily stretch and to be one-size-fits-all, both measuring the size of the hand and estimating the finger joint motions of the thumb, index, and middle fingers. The system was calibrated and evaluated using comprehensive hand motion data that reflect the extensive range of natural human hand motions and various anatomical structures. The data were collected with a custom motion-capture setup and transformed into the joint angles through our post-processing method. The glove system is capable of reconstructing arbitrary and even unconventional hand poses with accuracy and robustness, confirmed by evaluations on the estimation of bone lengths (mean error: 2.1 mm), joint angles (mean error: 4.16°), and fingertip positions (mean 3D error: 4.02 mm), and on overall hand pose reconstructions in various applications. The proposed glove allows us to take advantage of the dexterity of the human hand with potential applications, including but not limited to teleoperation of anthropomorphic robot hands or surgical robots, virtual and augmented reality, and collection of human motion data.
β-amyloid monomer scavenging by an anticalin protein prevents neuronal hyperactivity in mouse models of Alzheimer’s Disease
Authors: Zott Benedikt , Nästle Lea , Grienberger Christine , Unger Felix , Knauer Manuel M. , Wolf Christian , Keskin-Dargin Aylin , Feuerbach Anna , Busche Marc Aurel , Skerra Arne , Konnerth Arthur 
Published: July 2024

AbstractHyperactivity mediated by synaptotoxic β-amyloid (Aβ) oligomers is one of the earliest forms of neuronal dysfunction in Alzheimer’s disease. In the search for a preventive treatment strategy, we tested the effect of scavenging Aβ peptides before Aβ plaque formation. Using in vivo two-photon calcium imaging and SF-iGluSnFR-based glutamate imaging in hippocampal slices, we demonstrate that an Aβ binding anticalin protein (Aβ-anticalin) can suppress early neuronal hyperactivity and synaptic glutamate accumulation in the APP23xPS45 mouse model of β-amyloidosis. Our results suggest that the sole targeting of Aβ monomers is sufficient for the hyperactivity-suppressing effect of the Aβ-anticalin at early disease stages. Biochemical and neurophysiological analyses indicate that the Aβ-anticalin-dependent depletion of naturally secreted Aβ monomers interrupts their aggregation to neurotoxic oligomers and, thereby, reverses early neuronal and synaptic dysfunctions. Thus, our results suggest that Aβ monomer scavenging plays a key role in the repair of neuronal function at early stages of AD.
High-density vertical sidewall MoS2 transistors through T-shape vertical lamination
Authors: Tao Quanyang , Wu Ruixia , Zou Xuming , Chen Yang , Li Wanying , Lu Zheyi , Ma Likuan , Kong Lingan , Lu Donglin , Yang Xiaokun , Song Wenjing , Li Wei , Liu Liting , Ding Shuimei , Liu Xiao , Duan Xidong , Liao Lei , Liu Yuan 
Published: July 2024

AbstractVertical transistors, in which the source and drain are aligned vertically and the current flow is normal to the wafer surface, have attracted considerable attention recently. However, the realization of high-density vertical transistors is challenging, and could be largely attributed to the incompatibility between vertical structures and conventional lateral fabrication processes. Here we report a T-shape lamination approach for realizing high-density vertical sidewall transistors, where lateral transistors could be pre-fabricated on planar substrates first and then laminated onto vertical substrates using T-shape stamps, hence overcoming the incompatibility between planar processes and vertical structures. Based on this technique, we vertically stacked 60 MoS2transistors within a small vertical footprint, corresponding to a device density over 108 cm−2. Furthermore, we demonstrate two approaches for scalable fabrication of vertical sidewall transistor arrays, including simultaneous lamination onto multiple vertical substrates, as well as on the same vertical substrate using multi-cycle layer-by-layer laminations.
Compartmentalized mitochondrial ferroptosis converges with optineurin-mediated mitophagy to impact airway epithelial cell phenotypes and asthma outcomes
Authors: Yamada Kazuhiro , St. Croix Claudette , Stolz Donna B. , Tyurina Yulia Y. , Tyurin Vladimir A. , Bradley Laura R. , Kapralov Alexander A. , Deng Yanhan , Zhou Xiuxia , Wei Qi , Liao Bo , Fukuda Nobuhiko , Sullivan Mara , Trudeau John , Ray Anuradha , Kagan Valerian E. , Zhao Jinming , Wenzel Sally E. 
Published: July 2024

AbstractA stable mitochondrial pool is crucial for healthy cell function and survival. Altered redox biology can adversely affect mitochondria through induction of a variety of cell death and survival pathways, yet the understanding of mitochondria and their dysfunction in primary human cells and in specific disease states, including asthma, is modest. Ferroptosis is traditionally considered an iron dependent, hydroperoxy-phospholipid executed process, which induces cytosolic and mitochondrial damage to drive programmed cell death. However, in this report we identify a lipoxygenase orchestrated, compartmentally-targeted ferroptosis-associated peroxidation process which occurs in a subpopulation of dysfunctional mitochondria, without promoting cell death. Rather, this mitochondrial peroxidation process tightly couples with PTEN-induced kinase (PINK)−1(PINK1)-Parkin-Optineurin mediated mitophagy in an effort to preserve the pool of functional mitochondria and prevent cell death. These combined peroxidation processes lead to altered epithelial cell phenotypes and loss of ciliated cells which associate with worsened asthma severity. Ferroptosis-targeted interventions of this process could preserve healthy mitochondria, reverse cell phenotypic changes and improve disease outcomes.
Brainstem Dbh+ neurons control allergen-induced airway hyperreactivity
Authors: Su Yujuan , Xu Jinhao , Zhu Ziai , Chin Jisun , Xu Le , Yu Haoze , Nudell Victoria , Dash Barsha , Moya Esteban A. , Ye Li , Nimmerjahn Axel , Sun Xin 
Published: July 2024

AbstractExaggerated airway constriction triggered by repeated exposure to allergen, also called hyperreactivity, is a hallmark of asthma. Whereas vagal sensory neurons are known to function in allergen-induced hyperreactivity1–3, the identity of downstream nodes remains poorly understood. Here we mapped a full allergen circuit from the lung to the brainstem and back to the lung. Repeated exposure of mice to inhaled allergen activated the nuclei of solitary tract (nTS) neurons in a mast cell-, interleukin-4 (IL-4)- and vagal nerve-dependent manner. Single-nucleus RNA sequencing, followed by RNAscope assay at baseline and allergen challenges, showed that a Dbh+ nTS population is preferentially activated. Ablation or chemogenetic inactivation of Dbh+ nTS neurons blunted hyperreactivity whereas chemogenetic activation promoted it. Viral tracing indicated that Dbh+ nTS neurons project to the nucleus ambiguus (NA) and that NA neurons are necessary and sufficient to relay allergen signals to postganglionic neurons that directly drive airway constriction. Delivery of noradrenaline antagonists to the NA blunted hyperreactivity, suggesting noradrenaline as the transmitter between Dbh+ nTS and NA. Together, these findings provide molecular, anatomical and functional definitions of key nodes of a canonical allergen response circuit. This knowledge informs how neural modulation could be used to control allergen-induced airway hyperreactivity.
The quantum transition of the two-dimensional Ising spin glass
Authors: Bernaschi Massimo , González-Adalid Pemartín Isidoro , Martín-Mayor Víctor , Parisi Giorgio 
Published: July 2024

AbstractQuantum annealers are commercial devices that aim to solve very hard computational problems1, typically those involving spin glasses2,3. Just as in metallurgic annealing, in which a ferrous metal is slowly cooled4, quantum annealers seek good solutions by slowly removing the transverse magnetic field at the lowest possible temperature. Removing the field diminishes the quantum fluctuations but forces the system to traverse the critical point that separates the disordered phase (at large fields) from the spin-glass phase (at small fields). A full understanding of this phase transition is still missing. A debated, crucial question regards the closing of the energy gap separating the ground state from the first excited state. All hopes of achieving an exponential speed-up, compared to classical computers, rest on the assumption that the gap will close algebraically with the number of spins5–9. However, renormalization group calculations predict instead that there is an infinite-randomness fixed point10. Here we solve this debate through extreme-scale numerical simulations, finding that both parties have grasped parts of the truth. Although the closing of the gap at the critical point is indeed super-algebraic, it remains algebraic if one restricts the symmetry of possible excitations. As this symmetry restriction is experimentally achievable (at least nominally), there is still hope for the quantum annealing paradigm11–13.
Prognostic value of Maspin protein level in patients with triple negative breast cancer
Authors: do Nascimento Renan Gomes , da Conceição Mércia Patrícia Ferreira , de Bastos Daniel Rodrigues , de Toledo Osorio Cynthia Aparecida Bueno , López Rossana Verónica Mendoza , Reis Eduardo Moraes , Cerqueira Otto Luiz Dutra 
Published: July 2024

AbstractThe search for prognostic markers in breast cancer has bumped into a typical feature of these tumors, intra and intertumoral heterogeneity. Changes in the expression profile, localization of these proteins or shedding to the surrounding stroma can be useful in the search for new markers. In this context, classification by molecular subtypes can bring perspectives for both diagnosis and screening for appropriate treatments. However, the Triple Negative (TN) subtype, which is already the one with the worst prognosis, lacks appropriate and consistent molecular markers. In this work, we analyzed 346 human breast cancer samples in tissue microarrays (TMA) from cases diagnosed with invasive breast carcinoma to assess the expression and localization pattern of Maspin and their correlation with clinical parameters. To complement our findings, we also used TCGA data to analyze the mRNA levels of these respective genes. Our data suggests that the TN subtype demonstrates a higher level of cytoplasmic Maspin compared to the other subtypes. Maspin transcript levels follow the same trend. However, TN patients with lower Maspin expression tend to have worse overall survival and free-survival metastasis rates. Finally, we used Maspin expression data to verify possible relationships with the clinicopathological information of our cohort. Our univariate analyses indicate that Maspin is related to the expression of estrogen receptor (ER) and progesterone receptor (PR). Furthermore, Maspin expression levels also showed correlation with Scarff-Bloom-Richardson (SBR) parameter, and stromal Maspin showed a relationship with lymph node involvement. Our data is not consistently robust enough to categorize Maspin as a prognostic marker. However, it does indicate a change in the expression profile within the TN subtype.
Estimation of the UV susceptibility of aerosolized SARS-CoV-2 to 254 nm irradiation using CFD-based room disinfection simulations
Authors: van der Schans Marc , Yu Joan , de Vries Adrie , Martin Genevieve 
Published: July 2024

AbstractThe recent COVID-19 pandemic has raised interest in efficient air disinfection solutions. The application of germicidal ultraviolet (GUV) irradiation is an excellent contender to prevent airborne transmission of COVID-19, as well as other existing and future infectious airborne diseases. While GUV has already been proven effective in inactivating SARS-CoV-2, quantitative data on UV susceptibility and dose requirements, needed to predict and optimize the performance of GUV solutions, is still limited. In this study, the UV susceptibility of aerosolized SARS-CoV-2 to 254 nm ultraviolet (UV) irradiation is investigated. This is done by employing 3D computational fluid dynamics based simulations of SARS-CoV-2 inactivation in a test chamber equipped with an upper-room UV-C luminaire and comparing the results to previously published measurements performed in the same test chamber. The UV susceptibility found in this study is (0.6 ± 0.2) m2/J, which is equivalent to a D90 dose between 3 and 6 J/m2. These values are in the same range as previous estimations based on other corona viruses and inactivation data reported in literature.
Quantifiable and reproducible phenotypic assessment of a constitutive knockout mouse model for congenital nephrotic syndrome of the Finnish type
Authors: Lemberg Katharina , Mertens Nils D. , Yousef Kirollos , Schneider Ronen , Merz Lea M. , Mansour Bshara , Salmanullah Daanya , Kolvenbach Caroline M. , Saida Ken , Yu Seyoung , Hölzel Selina , Steinsapir Andrew , Goncalves Kevin A. , Nicolas Frank Camille , Franken Gijs A. C. , Shril Shirlee , Buerger Florian , Hildebrandt Friedhelm 
Published: July 2024

AbstractSteroid-resistant nephrotic syndrome (SRNS) is the second most frequent cause of childhood chronic kidney disease. Congenital nephrotic syndrome of the Finnish type (CNF) (MIM# 256300) is caused by biallelic variants in the gene NPHS1, encoding nephrin, an integral component of the kidney filtration barrier. No causal treatments exist, and children inevitably require kidney replacement therapy. In preparation for gene replacement therapy (GRT) in CNF, we established a quantifiable and reproducible phenotypic assessment of the nephrin-deficient CNF mouse model: 129/Sv-Nphs1tm1Rkl/J. We assessed the phenotypic spectrum of homozygous mice (Nphs1tm1Rkl/Nphs1tm1Rkl) compared to heterozygous controls (Nphs1tm1Rkl/Nphs1WT) by the following parameters: 1. cohort survival, 2. podocyte foot process (FP) density per glomerular basement membrane (GBM) using transmission electron microscopy, 3. tubular microcysts in brightfield microscopy, and 4. urinary albumin/creatinine ratios. Nphs1tm1Rkl/Nphs1tm1Rkl mice exhibited: 1. perinatal lethality with median survival of 1 day, 2. FP effacement with median FP density of 1.00 FP/µm GBM (2.12 FP/µm in controls), 3. tubular dilation with 65 microcysts per section (6.5 in controls), and 4. increased albumin/creatinine ratio of 238 g/g (4.1 g/g in controls). We here established four quantifiable phenotyping features of a CNF mouse model to facilitate future GRT studies by enabling sensitive detection of phenotypic improvements.
Stent coating containing a charged silane coupling agent that regulates protein adsorption to confer antithrombotic and cell-adhesion properties
Authors: Inuzuka Naoki , Shobayashi Yasuhiro , Tateshima Satoshi , Sato Yuya , Ohba Yoshio , Ekdahl Kristina N. , Nilsson Bo , Teramura Yuji 
Published: July 2024

AbstractThe evolution of endovascular therapies, particularly in the field of intracranial aneurysm treatment, has been truly remarkable and is characterized by the development of various stents. However, ischemic complications related to thrombosis or downstream emboli pose a challenge for the broader clinical application of such stents. Despite advancements in surface modification technologies, an ideal coating that fulfills all the desired requirements, including anti-thrombogenicity and swift endothelialization, has not been available. To address these issues, we investigated a new coating comprising 3-aminopropyltriethoxysilane (APTES) with both anti-thrombogenic and cell-adhesion properties. We assessed the anti-thrombogenic property of the coating using an in vitro blood loop model by evaluating the platelet count and the level of the thrombin–antithrombin (TAT) complex, and investigating thrombus formation on the surface using scanning electron microscopy (SEM). We then assessed endothelial cell adhesion on the metal surfaces. In vitro blood tests revealed that, compared to a bare stent, the coating significantly inhibited platelet reduction and thrombus formation; more human serum albumin spontaneously adhered to the coated surface to block thrombogenic activation in the blood. Cell adhesion tests also indicated a significant increase in the number of cells adhering to the APTES-coated surfaces compared to the numbers adhering to either the bare stent or the stent coated with an anti-fouling phospholipid polymer. Finally, we performed an in vivo safety test by implanting coated stents into the internal thoracic arteries and ascending pharyngeal arteries of minipigs, and subsequently assessing the health status and vessel patency of the arteries by angiography over the course of 1 week. We found that there were no adverse effects on the pigs and the vascular lumens of their vessels were well maintained in the group with APTES-coated stents. Therefore, our new coating exhibited both high anti-thrombogenicity and cell-adhesion properties, which fulfill the requirements of an implantable stent.
A whole-genome CRISPR screen identifies the spindle accessory checkpoint as a locus of nab-paclitaxel resistance in a pancreatic cancer cell line
Authors: Mondal Priya , Alyateem George , Mitchell Allison V. , Gottesman Michael M. 
Published: July 2024

AbstractPancreatic adenocarcinoma is one of the most aggressive and lethal forms of cancer. Chemotherapy is the primary treatment for pancreatic cancer, but resistance to the drugs used remains a major challenge. A genome-wide CRISPR interference and knockout screen in the PANC-1 cell line with the drug nab-paclitaxel has identified a group of spindle assembly checkpoint (SAC) genes that enhance survival in nab-paclitaxel. Knockdown of these SAC genes (BUB1B, BUB3, and TTK) attenuates paclitaxel-induced cell death. Cells treated with the small molecule inhibitors BAY 1217389 or MPI 0479605, targeting the threonine tyrosine kinase (TTK), also enhance survival in paclitaxel. Overexpression of these SAC genes does not affect sensitivity to paclitaxel. These discoveries have helped to elucidate the mechanisms behind paclitaxel cytotoxicity. The outcomes of this investigation may pave the way for a deeper comprehension of the diverse responses of pancreatic cancer to therapies including paclitaxel. Additionally, they could facilitate the formulation of novel treatment approaches for pancreatic cancer.
Initiating-clone analysis in patients with acute myeloid leukemia secondary to essential thrombocythemia
Authors: Ushijima Yoko , Naruse Seara , Ishikawa Yuichi , Kawashima Naomi , Sanada Masashi , Nakashima Marie , Kim Jeong Hui , Terakura Seitaro , Kihara Rika , Watamoto Koichi , Nishiyama Takahiro , Kitamura Kunio , Matsushita Tadashi , Kiyoi Hitoshi 
Published: July 2024

AbstractMost of essential thrombocythemia (ET) patients have the clone harboring a mutation in one of the JAK2, CALR, or MPL gene, and these clones generally acquire additional mutations at transformation to acute myeloid leukemia (AML). However, the proliferation of triple-negative clones has sometimes been observed at AML transformation. To clarify the clonal evolution of ET to AML, we analyzed paired samples at ET and AML transformation in eight patients. We identified that JAK2-unmutated AML clones proliferated at AML transformation in three patients in whom the JAK2-mutated clone was dominant at ET. In two patients, TET2-mutated, but not JAK2-mutated, clones might be common initiating clones for ET and transformed AML. In a patient with JAK2-mutated ET, SMARCC2, UBR4, and ZNF143, but not JAK2, -mutated clones proliferated at AML transformation. Precise analysis using single-cell sorted CD34+/CD38- fractions suggested that ET clone with JAK2-mutated and AML clone with TP53 mutation was derived from the common clone with these mutations. Although further study is required to clarify the biological significance of SMARCC2, UBR4, and ZNF143 mutations during disease progression of ET and AML transformation, the present results demonstrate the possibility of a common initial clone involved in both ET and transformed AML.
Combination of error-prone PCR (epPCR) and Circular Polymerase Extension Cloning (CPEC) for improving the coverage of random mutagenesis libraries
Authors: Ossa-Hernández Natalia , Marins Luis Fernando , Almeida Daniela Volcan 
Published: July 2024

AbstractRandom mutagenesis, such as error-prone PCR (epPCR), is a technique capable of generating a wide variety of a single gene. However, epPCR can produce a large number of mutated gene variants, posing a challenge in ligating these mutated PCR products into plasmid vectors. Typically, the primers for mutagenic PCRs incorporate artificial restriction enzyme sites compatible with chosen plasmids. Products are cleaved and ligated to linearized plasmids, then recircularized by DNA ligase. However, this cut-and-paste method known as ligation-dependent process cloning (LDCP), has limited efficiency, as the loss of potential mutants is inevitable leading to a significant reduction in the library’s breadth. An alternative to LDCP is the circular polymerase extension cloning (CPEC) method. This technique involves a reaction where a high-fidelity DNA polymerase extends the overlapping regions between the insert and vector, forming a circular molecule. In this study, our objective was to compare the traditional cut-and-paste enzymatic method with CPEC in producing a variant library from the gene encoding the red fluorescent protein (DsRed2) obtained by epPCR. Our findings suggest that CPEC can accelerate the cloning process in gene library generation, enabling the acquisition of a greater number of gene variants compared to methods reliant on restriction enzymes.
Nano fuzzy alarming system for blood transfusion requirement detection in cancer using deep learning
Authors: Rady Raz Nasibeh , Anoushirvani Ali Arash , Rahimian Neda , Ghoerishi Maryam , Alibeik Nazanin , Sajadi Rad Masoumeh 
Published: July 2024

AbstractPeriodic blood transfusion is a need in cancer patients in which the disease process as well as the chemotherapy can disrupt the natural production of blood cells. However, there are concerns about blood transfusion side effects, the cost, and the availability of donated blood. Therefore, predicting the timely requirement for blood transfusion considering patient variability is a need, and here for the first-time deal with this issue in blood cancer using in vivo data. First, a data set of 98 samples of blood cancer patients including 61 features of demographic, clinical, and laboratory data are collected. After performing multivariate analysis and the approval of an expert, effective parameters are derived. Then using a deep recurrent neural network, a system is presented to predict a need for packed red blood cell transfusion. Here, we use a Long Short-Term Memory (LSTM) neural network for modeling and the cross-validation technique with 5 layers for validation of the model along with comparing the result with networking and non-networking machine learning algorithms including bidirectional LSTM, AdaBoost, bagging decision tree based, bagging KNeighbors, and Multi-Layer Perceptron (MLP). Results show the LSTM outperforms the other methods. Then, using the swarm of fuzzy bioinspired nanomachines and the most effective parameters of Hgb, PaO2, and pH, we propose a feasibility study on nano fuzzy alarming system (NFABT) for blood transfusion requirements. Alarming decisions using the Internet of Things (IoT) gateway are delivered to the physician for performing medical actions. Also, NFABT is considered a real-time non-invasive AI-based hemoglobin monitoring and alarming method. Results show the merits of the proposed method.