bluuebunny/crossref_metadata_2025_split huggingface dataset:
Upper Plate Structure and Megathrust Properties in the Shumagin Gap Near the July 2020 M7.8 Simeonof Event
Authors: Shillington Donna J. , Bécel Anne , Nedimović Mladen R. 
Published: January 2022

AbstractSubduction zone architecture and properties are thought to control megathrust slip behavior, but few constraints on crustal structure and megathrust properties are available at sufficient resolution and depth, hindering understanding of linkages between structure and behavior. Here we present a P‐wave seismic velocity model based on wide‐angle seismic data integrated with collocated reflection imaging in the weakly coupled Shumagin Gap in the Alaska subduction zone, where a M7.8 occurred in July 2020. We show that this earthquake occurred near and below the Moho of the overriding plate where the megathrust is characterized by a 3‐ to 5‐km‐thick reflection band interpreted to represent tectonic mixing. The rheological heterogeneity of the plate boundary near and below the Moho could account for abundant interplate seismicity, repeated M7.x events, and patchiness of the 2020 rupture. Velocity variations in the overriding continental crust imply changes in rigidity that could further influence megathrust slip.
Laboratory Simulation of Solar Wind Interaction With Lunar Magnetic Anomalies
Authors: Yeo Li Hsia , Han Jia , Wang Xu , Werner Greg , Deca Jan , Munsat Tobin , Horányi Mihály 
Published: January 2022

AbstractMagnetic anomalies on the surface of the Moon interact with the solar wind plasma flow, resulting in both magnetic and electrostatic deflection/reflection of charged particles. Consequently, surface charging in these regions differs from regions without magnetic fields. Using the Colorado Solar Wind Experiment facility, this interaction is investigated with high‐energy flowing plasmas (100–800 eV beam ions) that are incident upon a magnetic dipole embedded beneath an insulating surface. The dipole moment is perpendicular to the surface. The plasma potential distribution is measured above the surface using an emissive probe. In the dipole lobe regions the surface is charged to significantly higher positive potentials by the un‐magnetized ion beam impinging on the surface while the electrons remain excluded by the magnetic field. At low ion beam energies the results agree with these expectations as the surface potential follows the ion beam energy. However, at high beam energies, the surface potentials in the electron‐shielded lobe regions remain significantly lower than the expected magnitude. Surprisingly, electrons are detected in the shielded regions by a Langmuir probe. A test particle simulation indicates that secondary electrons induced by the high energy ion beams impinging on the surface can enter the shielded regions, thus lowering the surface potential.
Segmentation of Shallow Slow Slip Events at the Hikurangi Subduction Zone Explained by Along‐Strike Changes in Fault Geometry and Plate Convergence Rates
Authors: Perez‐Silva Andrea , Kaneko Yoshihiro , Savage Martha , Wallace Laura , Li Duo , Williams Charles 
Published: January 2022

AbstractOver the last two decades, geodetic and seismic observations have revealed a spectrum of slow earthquakes along the Hikurangi subduction zone in New Zealand. Of those, shallow slow slip events (SSEs) that occur at depths of less than 15 km along the plate interface show a strong along‐strike segmentation in their recurrence intervals, which vary from ∼1 yr from offshore Tolaga Bay in the northeast to ∼5 yr offshore Cape Turnagain ∼300 km to the southwest. To understand the factors that control this segmentation, we conduct numerical simulations of SSEs incorporating laboratory‐derived rate‐and‐state friction laws with both planar and non‐planar fault geometries. We find that a relatively simple model assuming a realistic non‐planar fault geometry reproduces the characteristics of shallow SSEs as constrained by geodetic observations. Our preferred model captures the magnitudes and durations of SSEs, as well as the northward decrease of their recurrence intervals. Our results indicate that the segmentation of SSE recurrence intervals is favored by along‐strike changes in both the plate convergence rate and the downdip width of the SSE source region. Modeled SSEs with longer recurrence intervals concentrate in the southern part of the fault (offshore Cape Turnagain), where the plate convergence rate is lowest and the source region of SSEs is widest due to the shallower slab dip angle. Notably, the observed segmentation of shallow SSEs cannot be reproduced with a simple planar fault model, which indicates that a realistic plate interface is an important factor to account for in modeling SSEs.
Martian Dust Storms and Gravity Waves: Disentangling Water Transport to the Upper Atmosphere
Authors: Shaposhnikov Dmitry S. , Medvedev Alexander S. , Rodin Alexander V. , Yiğit Erdal , Hartogh Paul 
Published: January 2022

AbstractSimulations with the Max Planck Institute Martian general circulation model for Martian years 28 and 34 reveal details of the water “pump” mechanism and the role of gravity wave (GW) forcing. Water is advected to the upper atmosphere mainly by upward branches of the meridional circulation: in low latitudes during equinoxes and over the south pole during solstices. Molecular diffusion plays little role in water transport in the middle atmosphere and across the mesopause. GWs modulate the circulation and temperature during global dust storms, thus changing the timing and intensity of the transport. At equinoxes, they facilitate water accumulation in the polar warming regions in the middle atmosphere followed by stronger upwelling over the equator. As equinoctial storms decay, GWs tend to accelerate the reduction of water in the thermosphere. GWs delay the onset of the transport during solstitial storms and change the globally averaged amount of water in the upper atmosphere by 10%–25%.
Identification of ∆9-tetrahydrocannabinol (THC) impairment using functional brain imaging
Authors: Gilman Jodi M. , Schmitt William A. , Potter Kevin , Kendzior Brian , Pachas Gladys N. , Hickey Sarah , Makary Meena , Huestis Marilyn A. , Evins A. Eden 
Published: January 2022

AbstractThe primary cannabinoid in cannabis, Δ9-tetrahydrocannabinol (THC), causes intoxication and impaired function, with implications for traffic, workplace, and other situational safety risks. There are currently no evidence-based methods to detect cannabis-impaired driving, and current field sobriety tests with gold-standard, drug recognition evaluations are resource-intensive and may be prone to bias. This study evaluated the capability of a simple, portable imaging method to accurately detect individuals with THC impairment. In this double-blind, randomized, cross-over study, 169 cannabis users, aged 18–55 years, underwent functional near-infrared spectroscopy (fNIRS) before and after receiving oral THC and placebo, at study visits one week apart. Impairment was defined by convergent classification by consensus clinical ratings and an algorithm based on post-dose tachycardia and self-rated “high.” Our primary outcome, prefrontal cortex (PFC) oxygenated hemoglobin concentration (HbO), was increased after THC only in participants operationalized as impaired, independent of THC dose. ML models using fNIRS time course features and connectivity matrices identified impairment with 76.4% accuracy, 69.8% positive predictive value (PPV), and 10% false-positive rate using convergent classification as ground truth, which exceeded Drug Recognition Evaluator-conducted expanded field sobriety examination (67.8% accuracy, 35.4% PPV, and 35.4% false-positive rate). These findings demonstrate that PFC response activation patterns and connectivity produce a neural signature of impairment, and that PFC signal, measured with fNIRS, can be used as a sole input to ML models to objectively determine impairment from THC intoxication at the individual level. Future work is warranted to determine the specificity of this classifier to acute THC impairment.ClinicalTrials.gov Identifier: NCT03655717
The POU2F1-ALDOA axis promotes the proliferation and chemoresistance of colon cancer cells by enhancing glycolysis and the pentose phosphate pathway activity
Authors: Lin Jinguan , Xia Longzheng , Oyang Linda , Liang Jiaxin , Tan Shiming , Wu Nayiyuan , Yi Pin , Pan Qing , Rao Shan , Han Yaqian , Tang Yanyan , Su Min , Luo Xia , Yang Yiqing , Chen Xiaohui , Yang Lixia , Zhou Yujuan , Liao Qianjin 
Published: January 2022

AbstractCancer metabolic reprogramming enhances its malignant behaviors and drug resistance, which is regulated by POU domain transcription factors. This study explored the effect of POU domain class 2 transcription factor 1 (POU2F1) on metabolic reprogramming in colon cancer. The POU2F1 expression was analyzed in GEO dataset, TCGA cohorts and human colon cancer tissues by bioinformatics and immunohistochemistry. The effects of altered POU2F1 expression on proliferation, glucose metabolism and oxaliplatin sensitivity of colon cancer cells were tested. The impacts of POU2F1 on aldolase A (ALDOA) expression and malignant behaviors of colon cancer cells were examined. We found that up-regulated POU2F1 expression was associated with worse prognosis and oxaliplatin resistance in colon cancer. POU2F1 enhanced the proliferation, aerobic glycolysis and the pentose phosphate pathway (PPP) activity, but reduced oxidative stress and apoptosis in colon cancer cells, dependent on up-regulating ALDOA expression. Mechanistically, POU2F1 directly bound to the ALDOA promoter to enhance the ALDOA promoter activity in colon cancer cells. Moreover, activation of the POU2F1-ALDOA axis decreased the sensitivity to oxaliplatin in colon cancer cells. These data indicate that the POU2F1-ALDOA axis promotes the progression and oxaliplatin resistance by enhancing metabolic reprogramming in colon cancer. Our findings suggest that the POU2F1-ALDOA axis may be new therapeutic targets to overcome oxaliplatin resistance in colon cancer.
Forest tree growth is linked to mycorrhizal fungal composition and function across Europe
Authors: Anthony Mark A , Crowther Thomas W , van der Linde Sietse , Suz Laura M , Bidartondo Martin I , Cox Filipa , Schaub Marcus , Rautio Pasi , Ferretti Marco , Vesterdal Lars , De Vos Bruno , Dettwiler Mike , Eickenscheidt Nadine , Schmitz Andreas , Meesenburg Henning , Andreae Henning , Jacob Frank , Dietrich Hans-Peter , Waldner Peter , Gessler Arthur , Frey Beat , Schramm Oliver , van den Bulk Pim , Hensen Arjan , Averill Colin 
Published: January 2022

Abstract
Most trees form symbioses with ectomycorrhizal fungi (EMF) which influence access to growth-limiting soil resources. Mesocosm experiments repeatedly show that EMF species differentially affect plant development, yet whether these effects ripple up to influence the growth of entire forests remains unknown. Here we tested the effects of EMF composition and functional genes relative to variation in well-known drivers of tree growth by combining paired molecular EMF surveys with high-resolution forest inventory data across 15 European countries. We show that EMF composition was linked to a three-fold difference in tree growth rate even when controlling for the primary abiotic drivers of tree growth. Fast tree growth was associated with EMF communities harboring high inorganic but low organic nitrogen acquisition gene proportions and EMF which form contact versus medium-distance fringe exploration types. These findings suggest that EMF composition is a strong bio-indicator of underlying drivers of tree growth and/or that variation of forest EMF communities causes differences in tree growth. While it may be too early to assign causality or directionality, our study is one of the first to link fine-scale variation within a key component of the forest microbiome to ecosystem functioning at a continental scale.
Immunological causes of obsessive-compulsive disorder: is it time for the concept of an “autoimmune OCD” subtype?
Authors: Endres Dominique , Pollak Thomas A. , Bechter Karl , Denzel Dominik , Pitsch Karoline , Nickel Kathrin , Runge Kimon , Pankratz Benjamin , Klatzmann David , Tamouza Ryad , Mallet Luc , Leboyer Marion , Prüss Harald , Voderholzer Ulrich , Cunningham Janet L. ,   ECNP Network Immuno-NeuroPsychiatry, Domschke Katharina , Tebartz van Elst Ludger , Schiele Miriam A. 
Published: January 2022

AbstractObsessive-compulsive disorder (OCD) is a highly disabling mental illness that can be divided into frequent primary and rarer organic secondary forms. Its association with secondary autoimmune triggers was introduced through the discovery of Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal infection (PANDAS) and Pediatric Acute onset Neuropsychiatric Syndrome (PANS). Autoimmune encephalitis and systemic autoimmune diseases or other autoimmune brain diseases, such as multiple sclerosis, have also been reported to sometimes present with obsessive-compulsive symptoms (OCS). Subgroups of patients with OCD show elevated proinflammatory cytokines and autoantibodies against targets that include the basal ganglia. In this conceptual review paper, the clinical manifestations, pathophysiological considerations, diagnostic investigations, and treatment approaches of immune-related secondary OCD are summarized. The novel concept of “autoimmune OCD” is proposed for a small subgroup of OCD patients, and clinical signs based on the PANDAS/PANS criteria and from recent experience with autoimmune encephalitis and autoimmune psychosis are suggested. Red flag signs for “autoimmune OCD” could include (sub)acute onset, unusual age of onset, atypical presentation of OCS with neuropsychiatric features (e.g., disproportionate cognitive deficits) or accompanying neurological symptoms (e.g., movement disorders), autonomic dysfunction, treatment resistance, associations of symptom onset with infections such as group A streptococcus, comorbid autoimmune diseases or malignancies. Clinical investigations may also reveal alterations such as increased levels of anti-basal ganglia or dopamine receptor antibodies or inflammatory changes in the basal ganglia in neuroimaging. Based on these red flag signs, the criteria for a possible, probable, and definite autoimmune OCD subtype are proposed.
Whole blood transcriptional signatures associated with rapid antidepressant response to ketamine in patients with treatment resistant depression
Authors: Cathomas Flurin , Bevilacqua Laura , Ramakrishnan Aarthi , Kronman Hope , Costi Sara , Schneider Molly , Chan Kenny L. , Li Long , Nestler Eric J. , Shen Li , Charney Dennis S. , Russo Scott J. , Murrough James W. 
Published: January 2022

AbstractKetamine has rapid and sustained antidepressant effects in patients with treatment-resistant depression (TRD). However, the underlying mechanisms of action are not well understood. There is increasing evidence that TRD is associated with a pro-inflammatory state and that ketamine may inhibit inflammatory processes. We thus investigated whole blood transcriptional profiles related to TRD and gene expression changes associated with treatment response to ketamine. Whole blood was collected at baseline (21 healthy controls [HC], 26 patients with TRD) and then again in patients with TRD 24 hours following a single intravenous infusion of ketamine (0.5 mg/kg). We performed RNA-sequencing and analyzed (a) baseline transcriptional profiles between patients with TRD and HC, (b) responders vs. non-responders before ketamine treatment, and (c) gene expression signatures associated with clinical improvement. At baseline, patients with TRD compared to HC showed a gene expression signature indicative of interferon signaling pathway activation. Prior to ketamine administration, the metabotropic glutamate receptor gene GRM2 and the ionotropic glutamate receptor gene GRIN2D were upregulated in responders compared to non-responders. Response to ketamine was associated with a distinct transcriptional signature, however, we did not observe gene expression changes indicative of an anti-inflammatory effect. Future studies are needed to determine the role of the peripheral immune system in the antidepressant effect of ketamine.
mGluR5 binding changes during a mismatch negativity task in a multimodal protocol with [11C]ABP688 PET/MR-EEG
Authors: Régio Brambilla Cláudia , Veselinović Tanja , Rajkumar Ravichandran , Mauler Jörg , Matusch Andreas , Ruch Andrej , Orth Linda , Ramkiran Shukti , Sbaihat Hasan , Kaulen Nicolas , Khudeish Nibal Yahya , Wyss Christine , Heekeren Karsten , Kawohl Wolfram , Rota Kops Elena , Tellmann Lutz , Scheins Jürgen , Boers Frank , Neumaier Bernd , Ermert Johannes , Lang Markus , Stüsgen Stefan , Herzog Hans , Langen Karl-Josef , Shah N. Jon , Lerche Christoph W. , Neuner Irene 
Published: January 2022

AbstractCurrently, the metabotropic glutamate receptor 5 (mGluR5) is the subject of several lines of research in the context of neurology and is of high interest as a target for positron-emission tomography (PET). Here, we assessed the feasibility of using [11C]ABP688, a specific antagonist radiotracer for an allosteric site on the mGluR5, to evaluate changes in glutamatergic neurotransmission through a mismatch-negativity (MMN) task as a part of a simultaneous and synchronized multimodal PET/MR-EEG study. We analyzed the effect of MMN by comparing the changes in nondisplaceable binding potential (BPND) prior to (baseline) and during the task in 17 healthy subjects by applying a bolus/infusion protocol. Anatomical and functional regions were analyzed. A small change in BPND was observed in anatomical regions (posterior cingulate cortex and thalamus) and in a functional network (precuneus) after the start of the task. The effect size was quantified using Kendall’s W value and was 0.3. The motor cortex was used as a control region for the task and did not show any significant BPND changes. There was a significant ΔBPND between acquisition conditions. On average, the reductions in binding across the regions were - 8.6 ± 3.2% in anatomical and - 6.4 ± 0.5% in the functional network (p ≤ 0.001). Correlations between ΔBPND and EEG latency for both anatomical (p = 0.008) and functional (p = 0.022) regions were found. Exploratory analyses suggest that the MMN task played a role in the glutamatergic neurotransmission, and mGluR5 may be indirectly modulated by these changes.
The effects of lisdexamfetamine dimesylate on eating behaviour and homeostatic, reward and cognitive processes in women with binge-eating symptoms: an experimental medicine study
Authors: Schneider Elizabeth , Martin Elizabeth , Rotshtein Pia , Qureshi Kasim L. , Chamberlain Samuel R. , Spetter Maartje S. , Dourish Colin T. , Higgs Suzanne 
Published: January 2022

AbstractLisdexamfetamine dimesylate (LDX) is the only drug currently approved by the FDA for the treatment of Binge-Eating Disorder (BED), but little is known about the behavioural mechanisms that underpin the efficacy of LDX in treating BED. We examined the behavioural and neural effects of an acute dose of LDX (50 mg) in 22 women with binge-eating symptomatology using a randomised, crossover, double-blind, placebo-controlled experimental medicine design. LDX reduced self-reported appetite ratings and intake of both a pasta meal and a palatable cookie snack. LDX also decreased the eating rate of pasta but not of cookies and reduced self-reported liking ratings for pasta at the end of the meal. When viewing food pictures during an fMRI scan, LDX reduced activity bilaterally in the thalamus. LDX enhanced sustained attention and reduced impulsive responding in a continuous performance task but had no effect on emotional bias or working memory. These results suggest the observed effects of LDX on food intake (and by implication the efficacy of LDX in treating BED) may be related to the actions of the drug to enhance satiety, reduce food-related reward responding when full and/or increase cognitive control. Novel pharmacotherapies for BED might be most effective if they have a broad spectrum of effects on appetite, reward and cognition.
Prenatal origins of suicide mortality: A prospective cohort study in the United States
Authors: Vidal-Ribas Pablo , Govender Theemeshni , Sundaram Rajeshwari , Perlis Roy H. , Gilman Stephen E. 
Published: January 2022

AbstractMost suicide research focuses on acute precipitants and is conducted in high-risk populations. Yet, vulnerability to suicide is likely established years prior to its occurrence. In this study, we aimed to investigate the risk of suicide mortality conferred by prenatal sociodemographic and pregnancy-related factors. Offspring of participants (N = 49,853) of the Collaborative Perinatal Project, a U.S. population-based cohort of pregnancies enrolled between 1959 and 1966, were linked to the U.S. National Death Index to determine their vital status by the end 2016. We examined associations between sociodemographic factors during pregnancy, pregnancy complications, labor and delivery complications, and neonatal complications with suicide death coded according to ICD-9/10 criteria. By the end of 2016, 3,555 participants had died. Of these, 288 (214 males, 74 females) died by suicide (incidence rate = 15.6 per 100,000 person-years, 95% Confidence Interval [CI] = 13.9–17.5). In adjusted models, male sex (Hazard Ratio [HR] = 2.98, CI: 2.26–3.93), White race (HR = 2.14, CI = 1.63–2.83), low parental education (HR = 2.23, CI = 1.38–3.62), manual parental occupation (HR = 1.38, CI = 1.05–1.82), being a younger sibling (HR = 1.52, CI = 1.10–2.11), higher rates of pregnancy complications (HR = 2.36, CI = 1.08–5.16), and smoking during pregnancy (HR = 1,28, CI = 0.99–1.66) were independently associated with suicide risk, whereas birth and neonatal complications were not. Consistent with the developmental origins of psychiatric disorders, vulnerability to suicide mortality is established early in development. Both sociodemographic and pregnancy factors play a role in this risk, which underscores the importance of considering life course approaches to suicide prevention, possibly including provision of high-quality prenatal care, and alleviating the socioeconomic burdens of mothers and families.