bluuebunny/crossref_metadata_2025_split huggingface dataset:
Single‐Stage Synchronous India‐Asia Collision Model Revealed by Himalayan High‐Pressure Metamorphic Rocks
Authors: Zhang Yanling , Yin Changqing , Ding Lin , Li Shun , Qian Jiahui , Gao Peng , Li Wangchao 
Published: August 2024

AbstractDespite a half‐century of intense research, the timing and diachroneity of initial collision between India and Asia remain highly debated, largely due to different definitions of “initial collision” and correspondingly different methods adopted. This study focuses on high‐pressure pelitic granulites of the Eastern Himalayan Syntaxis (EHS) to elucidate their metamorphic evolution and provide new constraints on the timing of initial India‐Asia collision. Petrological examination and phase equilibria modeling show that high‐pressure pelitic granulites have undergone four metamorphic stages, with the peak assemblage of garnet + K‐feldspar + kyanite + biotite ± plagioclase ± rutile + ilmenite + quartz at P‐T conditions of 13.1–15.7 kbar and 790–850°C. Clockwise P‐T paths suggest that the Indian continent underwent tectonometamorphic processes of initial collision and subsequent continent subduction. Zircon and monazite dating results indicate that the metamorphic ages of pelitic granulites range from 60 to 15 Ma, with the oldest ones clustered at 60–58 Ma. The oldest metamorphic ages of high‐ to ultrahigh‐pressure Himalayan metamorphic rocks can provide an upper age limit of the initial collision. Therefore, the initial India‐Asia collision must have occurred before 60–58 Ma in the EHS, roughly consistent with ca. 57 Ma in the western Himalaya and 63–60 Ma in the central Himalaya. Collectively, we conclude that the northern margin of India most likely underwent a single‐stage synchronous collision with the southern margin of Asia initially at around 60 Ma along the entire Yarlung‐Tsangpo suture zone.
Assessment of air quality in the Philadelphia, Pennsylvania subway
Authors: Karim Anjum Shahina , Malone Maeve , Bruno Alex , Eggler Aimee L. , Posner Michael A. , Shakya Kabindra M. 
Published: August 2024

Abstract
Background
Subways are popular and efficient modes of transportation in cities. However, people are exposed to high levels of particulate matter (PM) in subways. Subway air quality in the United States has been investigated in a few cities, but data is lacking on simultaneous measurement of several pollutants, especially ultrafine particles (UFP) and black carbon (BC), in combination with different size fractions of PM.

Objectives
The goals of this study are to assess air quality in a belowground subway and compare it with outdoor ambient levels, to examine temporal variability of PM in the subway, and to analyze the correlation between PM and BC.

Methods
Particulate matter of varying sizes (PM1, PM2.5, PM10), UFP, and BC were measured using DustTrak, nanoparticle detector, and micro aethalometer, respectively. Measurements were made at the belowground subway platform and the aboveground street level at 15th Street subway station in Philadelphia during summer 2022.

Results
Belowground mean PM1, PM2.5, and PM10 were 112.2 ± 61.3 µg/m3, 120 ± 65.5 µg/m3, and 182.1 ± 132 µg/m3, respectively, which were 5.4, 5.7, and 7.6 times higher than the respective aboveground street levels. The UFP lung deposited surface area (LDSA) (59.4 ± 36.2 µm2/cm3) and BC (9.5 ± 5.4 μg/m3) belowground were 1.7 times and 10.7 times higher than the aboveground. The pollutant concentration varied from day-to-day on both the locations. A higher positive correlation was found between the belowground BC and PM2.5 (r = 0.51, p < 0.05) compared to the aboveground (r = 0.16, p < 0.05).

Impact
This study showed high levels of particulate matter exposure at a belowground subway station in Philadelphia. Particulate matter levels were about 5 to 8 times higher at belowground subway station than the corresponding aboveground street level. Higher levels were also observed for UFP lung deposited surface area (LDSA), while black carbon levels showed the highest concentration at the belowground level by a factor of ten compared to the aboveground level. The study shows the need for air quality management at belowground subways to reduce particulate matter exposure for the commuters.
Effectiveness of biofeedback on blood pressure in patients with hypertension: systematic review and meta-analysis
Authors: Jenkins Sian , Cross Ainslea , Osman Hanad , Salim Farah , Lane Dan , Bernieh Dennis , Khunti Kamlesh , Gupta Pankaj 
Published: August 2024

AbstractHypertension is the leading modifiable risk factor for cardiovascular disease, but less than 50% have their blood pressure controlled. A possible avenue to support hypertension management is a holistic approach, using non-pharmacological interventions. Since hypertension is mediated in part by dysregulation of the autonomic nervous system (ANS), biofeedback may help improve hypertension management by targeted self-regulation and self-awareness of parameters that regulate the ANS. This systematic review aimed to assess the effectiveness of biofeedback on blood pressure in hypertensive patients. The review was pre-registered on PROSPERO and followed the PICO strategy. A total of 1782 articles were retrieved, 20 met the inclusion criteria. Sample sizes ranged from 15 to 301 participants; with a median age of 49.3 (43.3–55.0) years and 45% were female. There was a significant effect of biofeedback on systolic (−4.52, Z = 2.31, P = 0.02, CI [−8.35, −0.69]) and diastolic blood pressure (−5.19, Z = 3.54, P = 0.0004, CI [−8.07, −2.32]). Six different biofeedback modalities were used, with biofeedback delivered by psychologists, trained therapists and research assistants. There was no publication bias, heterogeneity was rated as substantial and data quality was rated to be poor. This review demonstrated that biofeedback had a significant effect on blood pressure. However, this should be viewed in the context of included studies being limited by heterogeneity and dated literature, meaning the research does not reflect the current biofeedback technology such as wearable devices. Future research should incorporate these technologies with robust methodology to fully understand the effect of biofeedback on hypertension.
AMDHD1 acts as a tumor suppressor and contributes to activation of TGF-β signaling pathway in cholangiocarcinoma
Authors: Ma Zuyi , Sun Jia , Li Zhenchong , Huang Shanzhou , Li Binglu 
Published: August 2024

Abstract
Cholangiocarcinoma (CCA) is a malignant tumor of the digestive system, characterized by its aggressive behavior and the absence of effective therapeutic biomarkers. Although recent studies have implicated AMDHD1 in tumor formation, its role in CCA development has been insufficiently explored. We utilized multiple bioinformatic datasets alongside 108 clinical samples to examine AMDHD1 expression in CCA. Then, in vitro and in vivo experiments were conducted to assess its impact on tumor growth and metastasis. Furthermore, proteomic analysis and immunoprecipitation mass spectrometry were employed to identify the downstream effectors of AMDHD1. We discovered that AMDHD1 was down-regulated in CCA and this down-regulation was associated with adverse clinicopathological features and prognosis. We also demonstrated that overexpression of AMDHD1 hindered G1/S progression in the cell cycle and promoted apoptosis, thereby inhibiting tumor growth and metastasis. Mechanistically, we found that AMDHD1 operated in a TGF-β-dependent manner and the inhibition of TGF-β signaling abrogated the effect of AMDHD1 overexpression on CCA cells. Specifically, AMDHD1 inhibited the ubiquitination and degradation of the SMAD4 protein through binding to the MH2 domain and synergistically enhanced SMAD2/3 phosphorylation, which activated of TGF-β signaling pathway and resulted in the suppression of CCA cell proliferation and migration. Our study identifies AMDHD1 as a significant prognostic biomarker and a tumor suppressor in CCA. It underscores the pivotal role of the AMDHD1/TGF-β signaling pathway in the development and progression of CCA.
Accurate de novo design of heterochiral protein–protein interactions
Authors: Sun Ke , Li Sicong , Zheng Bowen , Zhu Yanlei , Wang Tongyue , Liang Mingfu , Yao Yue , Zhang Kairan , Zhang Jizhong , Li Hongyong , Han Dongyang , Zheng Jishen , Coventry Brian , Cao Longxing , Baker David , Liu Lei , Lu Peilong 
Published: August 2024

AbstractAbiotic d-proteins that selectively bind to natural l-proteins have gained significant biotechnological interest. However, the underlying structural principles governing such heterochiral protein–protein interactions remain largely unknown. In this study, we present the de novo design of d-proteins consisting of 50–65 residues, aiming to target specific surface regions of l-proteins or l-peptides. Our designer d-protein binders exhibit nanomolar affinity toward an artificial l-peptide, as well as two naturally occurring proteins of therapeutic significance: the D5 domain of human tropomyosin receptor kinase A (TrkA) and human interleukin-6 (IL-6). Notably, these d-protein binders demonstrate high enantiomeric specificity and target specificity. In cell-based experiments, designer d-protein binders effectively inhibited the downstream signaling of TrkA and IL-6 with high potency. Moreover, these binders exhibited remarkable thermal stability and resistance to protease degradation. Crystal structure of the designed heterochiral d-protein–l-peptide complex, obtained at a resolution of 2.0 Å, closely resembled the design model, indicating that the computational method employed is highly accurate. Furthermore, the crystal structure provides valuable information regarding the interactions between helical l-peptides and d-proteins, particularly elucidating a novel mode of heterochiral helix–helix interactions. Leveraging the design of d-proteins specifically targeting l-peptides or l-proteins opens up avenues for systematic exploration of the mirror-image protein universe, paving the way for a diverse range of applications.
Standardized wireless deep brain stimulation system for mice
Authors: Grotemeyer Alexander , Petschner Tobias , Peach Robert , Hoehl Dirk , Knauer Torsten , Thomas Uwe , Endres Heinz , Blum Robert , Sendtner Michael , Volkmann Jens , Ip Chi Wang 
Published: August 2024

AbstractDeep brain stimulation (DBS) has emerged as a revolutionary technique for accessing and modulating brain circuits. DBS is used to treat dysfunctional neuronal circuits in neurological and psychiatric disorders. Despite over two decades of clinical application, the fundamental mechanisms underlying DBS are still not well understood. One reason is the complexity of in vivo electrical manipulation of the central nervous system, particularly in rodent models. DBS-devices for freely moving rodents are typically custom-designed and not commercially available, thus making it difficult to perform experimental DBS according to common standards. Addressing these challenges, we have developed a novel wireless microstimulation system for deep brain stimulation (wDBS) tailored for rodents. We demonstrate the efficacy of this device for the restoration of behavioral impairments in hemiparkinsonian mice through unilateral wDBS of the subthalamic nucleus. Moreover, we introduce a standardized and innovative pipeline, integrating machine learning techniques to analyze Parkinson’s disease-like and DBS-induced gait changes.
Mitigation of interfacial dielectric loss in aluminum-on-silicon superconducting qubits
Authors: Biznárová Janka , Osman Amr , Rehnman Emil , Chayanun Lert , Križan Christian , Malmberg Per , Rommel Marcus , Warren Christopher , Delsing Per , Yurgens August , Bylander Jonas , Fadavi Roudsari Anita 
Published: August 2024

AbstractWe demonstrate aluminum-on-silicon planar transmon qubits with time-averaged T1 energy relaxation times of up to 270 μs, corresponding to Q = 5 million, and a highest observed value of 501 μs. Through materials analysis techniques and numerical simulations we investigate the dominant source of energy loss, and devise and demonstrate a strategy toward its mitigation. Growing aluminum films thicker than 300 nm reduces the presence of oxide, a known host of defects, near the substrate-metal interface, as confirmed by time-of-flight secondary ion mass spectrometry. A loss analysis of coplanar waveguide resonators shows that this results in a reduction of dielectric loss due to two-level system defects. The correlation between the enhanced performance of our devices and the film thickness is due to the aluminum growth in columnar structures of parallel grain boundaries: transmission electron microscopy shows larger grains in the thicker film, and consequently fewer grain boundaries containing oxide near the substrate-metal interface.
Crimean Congo hemorrhagic fever virus nucleoprotein and GP38 subunit vaccine combination prevents morbidity in mice
Authors: Karaaslan Elif , Sorvillo Teresa E. , Scholte Florine E. M. , O’Neal Troy Justin , Welch Stephen R. , Davies Katherine A. , Coleman-McCray JoAnn D. , Harmon Jessica R. , Ritter Jana M. , Pegan Scott D. , Montgomery Joel M. , Spengler Jessica R. , Spiropoulou Christina F. , Bergeron Éric 
Published: August 2024

AbstractImmunizing mice with Crimean-Congo hemorrhagic fever virus (CCHFV) nucleoprotein (NP), glycoprotein precursor (GPC), or with the GP38 domain of GPC, can be protective when the proteins are delivered with viral vectors or as a DNA or RNA vaccine. Subunit vaccines are a safe and cost-effective alternative to some vaccine platforms, but Gc and Gn glycoprotein subunit vaccines for CCHFV fail to protect despite eliciting high levels of neutralizing antibodies. Here, we investigated humoral and cellular immune responses and the protective efficacy of recombinant NP, GP38, and GP38 forms (GP85 and GP160) associated with the highly glycosylated mucin-like (MLD) domain, as well as the NP + GP38 combination. Vaccination with GP160, GP85, or GP38 did not confer protection, and vaccination with the MLD-associated GP38 forms blunted the humoral immune responses to GP38, worsened clinical chemistry, and increased viral RNA in the blood compared to the GP38 vaccination. In contrast, NP vaccination conferred 100% protection from lethal outcome and was associated with mild clinical disease, while the NP + GP38 combination conferred even more robust protection by reducing morbidity compared to mice receiving NP alone. Thus, recombinant CCHFV NP alone is a promising vaccine candidate conferring 100% survival against heterologous challenge. Moreover, incorporation of GP38 should be considered as it further enhances subunit vaccine efficacy by reducing morbidity in surviving animals.
Bacteria modulate microalgal aging physiology through the induction of extracellular vesicle production to remove harmful metabolites
Authors: Deng Yun , Yu Ruyi , Grabe Veit , Sommermann Thomas , Werner Markus , Vallet Marine , Zerfaß Christian , Werz Oliver , Pohnert Georg 
Published: August 2024

AbstractThe bloom and bust patterns of microalgae in aquatic systems contribute massively to global biogeochemical cycles. The decline of algal blooms is mainly caused by nutrient limitation resulting in cell death, the arrest of cell division and the aging of surviving cells. Nutrient intake can re-initiate proliferation, but the processes involved are poorly understood. Here we characterize how the bloom-forming diatom Coscinodiscus radiatus recovers from starvation after nutrient influx. Rejuvenation is mediated by extracellular vesicles that shuttle reactive oxygen species, oxylipins and other harmful metabolites out of the old cells, thereby re-enabling their proliferation. By administering nutrient pulses to aged cells and metabolomic monitoring of the response, we show that regulated pathways are centred around the methionine cycle in C. radiatus. Co-incubation experiments show that bacteria mediate aging processes and trigger vesicle production using chemical signalling. This work opens new perspectives on cellular aging and rejuvenation in complex microbial communities.
Unimolecular net heterolysis of symmetric and homopolar σ-bonds
Authors: Tiefel Anna F. , Grenda Daniel J. , Allacher Carina , Harrer Elias , Nagel Carolin H. , Kutta Roger J. , Hernández-Castillo David , Narasimhamurthy Poorva R. , Zeitler Kirsten , González Leticia , Rehbein Julia , Nuernberger Patrick , Breder Alexander 
Published: August 2024

AbstractThe unimolecular heterolysis of covalent σ-bonds is integral to many chemical transformations, including SN1-, E1- and 1,2-migration reactions. To a first approximation, the unequal redistribution of electron density during bond heterolysis is governed by the difference in polarity of the two departing bonding partners1–3. This means that if a σ-bond consists of two identical groups (that is, symmetric σ-bonds), its unimolecular fission from the S0, S1, or T1 states only occurs homolytically after thermal or photochemical activation1–7. To force symmetric σ-bonds into heterolytic manifolds, co-activation by bimolecular noncovalent interactions is necessary4. These tactics are only applicable to σ-bond constituents susceptible to such polarizing effects, and often suffer from inefficient chemoselectivity in polyfunctional molecules. Here we report the net heterolysis of symmetric and homopolar σ-bonds (that is, those with similar electronegativity and equal leaving group ability3) by means of stimulated doublet–doublet electron transfer (SDET). As exemplified by Se–Se and C–Se σ-bonds, symmetric and homopolar bonds initially undergo thermal homolysis, followed by photochemically SDET, eventually leading to net heterolysis. Two key factors make this process feasible and synthetically valuable: (1) photoexcitation probably occurs in only one of the incipient radical pair members, thus leading to coincidental symmetry breaking8 and consequently net heterolysis even of symmetric σ-bonds. (2) If non-identical radicals are formed, each radical may be excited at different wavelengths, thus rendering the net heterolysis highly chemospecific and orthogonal to conventional heterolyses. This feature is demonstrated in a series of atypical SN1 reactions, in which selenides show SDET-induced nucleofugalities3 rivalling those of more electronegative halides or diazoniums.
A hot-emitter transistor based on stimulated emission of heated carriers
Authors: Liu Chi , Wang Xin-Zhe , Shen Cong , Ma Lai-Peng , Yang Xu-Qi , Kong Yue , Ma Wei , Liang Yan , Feng Shun , Wang Xiao-Yue , Wei Yu-Ning , Zhu Xi , Li Bo , Li Chang-Ze , Dong Shi-Chao , Zhang Li-Ning , Ren Wen-Cai , Sun Dong-Ming , Cheng Hui-Ming 
Published: August 2024

AbstractHot-carrier transistors are a class of devices that leverage the excess kinetic energy of carriers. Unlike regular transistors, which rely on steady-state carrier transport, hot-carrier transistors modulate carriers to high-energy states, resulting in enhanced device speed and functionality. These characteristics are essential for applications that demand rapid switching and high-frequency operations, such as advanced telecommunications and cutting-edge computing technologies1–5. However, the traditional mechanisms of hot-carrier generation are either carrier injection6–11 or acceleration12,13, which limit device performance in terms of power consumption and negative differential resistance14–17. Mixed-dimensional devices, which combine bulk and low-dimensional materials, can offer different mechanisms for hot-carrier generation by leveraging the diverse potential barriers formed by energy-band combinations18–21. Here we report a hot-emitter transistor based on double mixed-dimensional graphene/germanium Schottky junctions that uses stimulated emission of heated carriers to achieve a subthreshold swing lower than 1 millivolt per decade beyond the Boltzmann limit and a negative differential resistance with a peak-to-valley current ratio greater than 100 at room temperature. Multi-valued logic with a high inverter gain and reconfigurable logic states are further demonstrated. This work reports a multifunctional hot-emitter transistor with significant potential for low-power and negative-differential-resistance applications, marking a promising advancement for the post-Moore era.
Mitochondrial complex I promotes kidney cancer metastasis
Authors: Bezwada Divya , Perelli Luigi , Lesner Nicholas P. , Cai Ling , Brooks Bailey , Wu Zheng , Vu Hieu S. , Sondhi Varun , Cassidy Daniel L. , Kasitinon Stacy , Kelekar Sherwin , Cai Feng , Aurora Arin B. , Patrick McKenzie , Leach Ashley , Ghandour Rashed , Zhang Yuanyuan , Do Duyen , McDaniel Phyllis , Sudderth Jessica , Dumesnil Dennis , House Sara , Rosales Tracy , Poole Alan M. , Lotan Yair , Woldu Solomon , Bagrodia Aditya , Meng Xiaosong , Cadeddu Jeffrey A. , Mishra Prashant , Garcia-Bermudez Javier , Pedrosa Ivan , Kapur Payal , Courtney Kevin D. , Malloy Craig R. , Genovese Giannicola , Margulis Vitaly , DeBerardinis Ralph J. 
Published: August 2024

AbstractMost kidney cancers are metabolically dysfunctional1–4, but how this dysfunction affects cancer progression in humans is unknown. We infused 13C-labelled nutrients in over 80 patients with kidney cancer during surgical tumour resection. Labelling from [U-13C]glucose varies across subtypes, indicating that the kidney environment alone cannot account for all tumour metabolic reprogramming. Compared with the adjacent kidney, clear cell renal cell carcinomas (ccRCCs) display suppressed labelling of tricarboxylic acid (TCA) cycle intermediates in vivo and in ex vivo organotypic cultures, indicating that suppressed labelling is tissue intrinsic. [1,2-13C]acetate and [U-13C]glutamine infusions in patients, coupled with measurements of respiration in isolated human kidney and tumour mitochondria, reveal lower electron transport chain activity in ccRCCs that contributes to decreased oxidative and enhanced reductive TCA cycle labelling. However, ccRCC metastases unexpectedly have enhanced TCA cycle labelling compared with that of primary ccRCCs, indicating a divergent metabolic program during metastasis in patients. In mice, stimulating respiration or NADH recycling in kidney cancer cells is sufficient to promote metastasis, whereas inhibiting electron transport chain complex I decreases metastasis. These findings in humans and mice indicate that metabolic properties and liabilities evolve during kidney cancer progression, and that mitochondrial function is limiting for metastasis but not growth at the original site.
Black holes regulate cool gas accretion in massive galaxies
Authors: Wang Tao , Xu Ke , Wu Yuxuan , Shi Yong , Elbaz David , Ho Luis C. , Zhang Zhi-Yu , Gu Qiusheng , Wang Yijun , Shu Chenggang , Yuan Feng , Xia Xiaoyang , Wang Kai 
Published: August 2024

AbstractThe nucleus of almost all massive galaxies contains a supermassive black hole (BH)1. The feedback from the accretion of these BHs is often considered to have crucial roles in establishing the quiescence of massive galaxies2–14, although some recent studies show that even galaxies hosting the most active BHs do not exhibit a reduction in their molecular gas reservoirs or star formation rates15–17. Therefore, the influence of BHs on galaxy star formation remains highly debated and lacks direct evidence. Here, based on a large sample of nearby galaxies with measurements of masses of both BHs and atomic hydrogen (HI), the main component of the interstellar medium18, we show that the HI gas mass to stellar masses ratio (μHI = MHI/M⋆) is more strongly correlated with BH masses (MBH) than with any other galaxy parameters, including stellar mass, stellar mass surface density and bulge masses. Moreover, once the μHI–MBH correlation is considered, μHI loses dependence on other galactic parameters, demonstrating that MBH serves as the primary driver of μHI. These findings provide important evidence for how the accumulated energy from BH accretion regulates the cool gas content in galaxies, by ejecting interstellar medium gas and/or suppressing gas cooling from the circumgalactic medium.