bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hales Discontinuity in the Southern Indian Continental Lithosphere: Seismological and Petrological Models
Authors: Chaudhury Jashodhara , Mitra Supriyo , Sarkar Tapabrato 
Published: January 2021

AbstractWe model the depth and Vs structure of the Hales discontinuity (H‐D) beneath Eastern Dharwar Craton (EDC) and Southern Granulite Terrain (SGT) using P wave receiver function (P‐RF) analysis and joint inversion with Rayleigh wave phase velocity dispersion. We calculate P‐RFs at higher frequency (fmax = 0.46 Hz), compared to previous studies, to show that the H‐D P‐to‐S converted phase (Phs) is distinct from crustal reverberations. Phs at stations Hyderabad (HYB) and Gauribidanur (GBA), in the EDC, arrive at ∼11.5 s and ∼12 s, respectively. From joint inversion, the H‐D is modeled at 107 ± 5 km and 113 ± 4 km depth, with ∼3% and ∼4% Vs increase, beneath HYB and GBA, respectively. For station Kodaikanal (KOD), in SGT, the Phs destructively interferes with the negative midcrustal reverberation at most ray‐parameters, which explains its apparent absence in previous studies. We isolated P‐RFs where Phs is distinct at ∼11 s and model it at 102 ± 3 km depth. Common conversion point stack profiles constructed by depth migrating P‐RFs through the Vs model show an undulatory nature of the H‐D. From data of mantle xenoliths (Wajrakarur kimberlite field), we calculate Vs of mantle peridotite and eclogite, using published bulk rock compositions. At the H‐D depth and temperature derived from Indian shield geotherm, we observed a good match to the Vs structure of the H‐D. Our results support the geodynamic model of the H‐D being an interface of paleosubducted eclogitic oceanic crust embedded within the upper mantle peridotite. Global observations of mantle reflectors within the continental lithosphere, at depths similar to H‐D, have been related to relict subduction and independently support our model.
Postbomb Subtropical North Pacific Surface Water Radiocarbon History
Authors: Guilderson Thomas P. , Schrag Daniel P. , Druffel Ellen R. M. , Reimer Ron W. 
Published: January 2021

AbstractWe have generated a high‐resolution coral Δ14C record from the leeward side of the Big Island of Hawai’i in the subtropical North Pacific. The record spans 1947–1992, when the coral was collected, and includes a brief prebomb interval as well as the postbomb era. Mean prebomb (1947–1954) values average −55‰ (±1, SE of the mean) with a clear seasonal cycle. Values are less positive during winter when vertical exchange mixes surface and lower‐14C subsurface waters. The postbomb annual maximum occurs in 1971 (+160‰) and decreases in a series of shifts to +105‰ in 1991, the end of our coral‐based reconstruction. The decrease is not monotonic and has inflection points during the La Niña years of 1973, 1977, and 1984. Imbedded in the Δ14C record is interannual variability in the El Nino‐Southern Oscillation band which is interpreted to reflect the lateral advection of low latitude surface waters as part of the oceanic Hadley Cell driven by Sverdrup dynamics.
Climatology and Evolution of the Antarctic Peninsula Föhn Wind‐Induced Melt Regime From 1979–2018
Authors: Laffin M. K. , Zender C. S. , Singh S. , Van Wessem J. M. , Smeets C. J. P. P. , Reijmer C. H. 
Published: January 2021

AbstractWarm and dry föhn winds on the Antarctic Peninsula (AP) cause surface melt that can destabilize vulnerable ice shelves. Topographic funneling of these downslope winds through mountain passes and canyons can produce localized wind‐induced melt that is difficult to quantify without direct measurements. Our Föhn Detection Algorithm (FöhnDA) identifies the surface föhn signature that causes melt from measurement by 12 Automatic Weather Stations on the AP, that train a machine learning model to detect föhn in 5 km Regional Atmospheric Climate Model 2 (RACMO2.3p2) simulations and in the ERA5 reanalysis model. We estimate the fraction of AP surface melt attributed to föhn and possibly katabatic winds and identify the drivers of melt, temporal variability, and long‐term trends and evolution from 1979–2018. We find that föhn wind‐induced melt accounts for 3.1% of the total melt on the AP and can be as high at 18% close to the mountains where the winds funnel through mountain canyons. Föhn‐induced surface melt does not significantly increase from 1979–2018, despite a warmer atmosphere and more positive Southern Annular Mode. However, a significant increase (+0.1 Gt y‐1) and subsequent decrease/stabilization occur in 1979–1998 and 1999–2018, consistent with the AP warming and cooling trends during the same time periods. Föhn occurrence, more than föhn strength, drives the annual variability in föhn‐induced melt. Long‐term föhn‐induced melt trends and evolution are attributable to seasonal changes in föhn occurrence, with increased occurrence in summer, and decreased occurrence in fall, winter, and early spring over the past 20 years.
Topographical Controls on Hillslope‐Scale Hydrology Drive Shrub Distributions on the Seward Peninsula, Alaska
Authors: Mekonnen Zelalem A. , Riley William J. , Grant Robert F. , Salmon Verity G. , Iversen Colleen M. , Biraud Sébastien C. , Breen Amy L. , Lara Mark J. 
Published: January 2021

AbstractObservations indicate shrubs are expanding across the Arctic tundra, mainly on hillslopes and primarily in response to climate warming. However, the impact topography exerts on hydrology, nutrient dynamics, and plant growth can make untangling the mechanisms behind shrub expansion difficult. We examined the role topography plays in determining shrub expansion by applying a coupled transect version of a mechanistic ecosystem model (ecosys) in a tundra hillslope site in the Seward Peninsula, Alaska. Modeled biomass of the dominant plant functional types agreed well with field measurements (R2 = 0.89) and accurately represented shrub expansion over the past 30 years inferred from satellite observations. In the well‐drained crest position, canopy water potential and plant nitrogen (N) uptake was modeled to be low from plant and microbial water stress. Intermediate soil water content in the mid‐slope position enhanced mineralization and plant N uptake, increasing shrub biomass. The deciduous shrub growth in the mid‐slope position was further enhanced by symbiotic N2 fixation primed by increased root carbon allocation. The gentle slope in the poorly drained lower‐slope position resulted in saturated soil conditions that reduced soil O2 concentrations, leading to lower root O2 uptake and lower nutrient uptake and plant biomass. A simulation that removed topographical interconnectivity between grid cells resulted in (1) a 28% underestimate of mean shrub biomass and (2) over or underestimated shrub productivity at the various hillslope positions. Our results indicate that land models need to account for hillslope‐scale coupled surface and subsurface hydrology to accurately predict current plant distributions and future trajectories in Arctic ecosystems.
Episodic Crustal Extension and Contraction Characterizing the Late Mesozoic Tectonics of East China: Evidence From the Jiaodong Peninsula, East China
Authors: Meng Lingtong , Lin Wei 
Published: January 2021

AbstractDuring the Late Mesozoic, East China is characterized by widespread magmatism, thrusting and folding, extensional doming, strike‐slip faulting, and block rotation. The Jiaodong Peninsula provides a key area located in East China to understand the episodic intracontinental extension and contraction and associated granitoid emplacement. Based on our structural analysis, magnetic fabric measurement, and gravity modeling, polyphase deformation and magma emplacement have been recognized within the Queshan‐Kunyushan‐Yuangezhuang‐Sanfoshan (QKYS) massif of the central Jiaodong Peninsula. A significant Late Jurassic D1 event, developed in the northern margin of the massif, was expressed by a high‐temperature, top‐to‐the‐NE shearing. Late Jurassic plutons display magnetic fabrics corresponding to the D1 structural fabrics and several NW–SE‐trending feeder zones at depth. These results link the syn‐kinematic emplacement of Late Jurassic plutons with regional NE–SW extensional tectonics. In the south of the massif, a lower‐temperature, top‐to‐the‐SW contractional deformation (D2) resulted from NE–SW contraction. The D3 shear zone with a top‐to‐the‐WNW kinematics is a rolling‐hinge type detachment fault that exhumed the massif, indicating NW–SE regional extension. Finally, Early Cretaceous plutons emplaced into the upper crust with a fast‐cooling rate and formed inverted drop shapes with concentric magnetic foliations and variably oriented magnetic lineations. In light of the previous geochronological results, the timing of these tectonic events is discussed. The tectonic evolution of the QKYS massif indicates a process from crustal thickening to lithospheric foundering in response to the Late Mesozoic plate convergences.
Lower amygdala fatty acid amide hydrolase in violent offenders with antisocial personality disorder: an [11C]CURB positron emission tomography study
Authors: Kolla Nathan J. , Boileau Isabelle , Karas Karolina , Watts Jeremy J. , Rusjan Pablo , Houle Sylvain , Mizrahi Romina 
Published: January 2021

AbstractAntisocial personality disorder (ASPD) imposes a high societal burden given the repetitive reactive aggression that affected individuals perpetrate. Since the brain endocannabinoid system (ECS) has been implicated in ASPD and aggressive behavior, we utilized [11C]CURB positron emission tomography to investigate fatty acid amide hydrolase (FAAH), an enzyme of the ECS that degrades anandamide, in 16 individuals with ASPD and 16 control participants. We hypothesized that FAAH density would be lower in the amygdala for several reasons. First, decreased FAAH expression is associated with increased cannabinoid receptor 1 stimulation, which may be responsible for amygdala hyper-reactivity in reactive aggression. Second, the amygdala is the seat of the neural circuit mediating reactive aggression. Third, other PET studies of externalizing populations show reduced brain FAAH density. Conversely, we hypothesized that FAAH expression would be greater in the orbitofrontal cortex. Consistent with our hypothesis, we found that amygdala FAAH density was lower in the amygdala of ASPD (p = 0.013). Cerebellar and striatal FAAH expression were inversely related with impulsivity (cerebellum: r = −0.60, p = 0.017; dorsal caudate: r = −0.58, p = 0.023; dorsal putamen: r = −0.55, p = 0.034), while cerebellar FAAH density was also negatively associated with assaultive aggression (r = −0.54, p = 0.035). ASPD presents high levels of disruptive behavior with few, if any, efficacious treatment options. Novel therapeutics that increase FAAH brain levels in a region-specific manner could hold promise for attenuating certain symptom clusters of ASPD, although our results require replication.
The IL-6 antagonist tocilizumab is associated with worse depression and related symptoms in the medically ill
Authors: Knight Jennifer M. , Costanzo Erin S. , Singh Suraj , Yin Ziyan , Szabo Aniko , Pawar Deepa S. , Hillard Cecilia J. , Rizzo J. Douglas , D’Souza Anita , Pasquini Marcelo , Coe Christopher L. , Irwin Michael R. , Raison Charles L. , Drobyski William R. 
Published: January 2021

AbstractBecause medical illness is associated with increased inflammation and an increased risk for treatment-resistant major depressive disorder, anti-cytokine therapy may represent a novel, and especially efficacious, treatment for depression. We hypothesized that blockade of the interleukin (IL)-6 signaling pathway with tocilizumab would decrease depression and related symptomatology in a longitudinal cohort of allogeneic hematopoietic stem cell transplantation (HCT) patients, a medically ill population with a significant inflammation and psychopathology. Patients undergoing allogeneic HCT received either a single dose of tocilizumab one day prior to HCT (n = 25), or HCT alone (n = 62). The primary outcome included depressive symptoms at 28 days post HCT; anxiety, fatigue, sleep, and pain were assessed at pretreatment baseline and days +28, +100, and +180 post HCT as secondary outcomes. Multivariate regression demonstrated that preemptive treatment with tocilizumab was associated with significantly higher depression scores at D28 vs. the comparison group (β = 5.74; 95% CI 0.75, 10.73; P = 0.03). Even after adjustment for baseline depressive symptoms, propensity score, and presence of acute graft-versus-host disease (grades II–IV) and other baseline covariates, the tocilizumab-exposed group continued to have significantly higher depression scores compared to the nonexposed group at D28 (β = 4.73; 95% CI 0.64, 8.81; P = 0.02). Despite evidence that IL-6 antagonism would be beneficial, blockade of the IL-6 receptor with tocilizumab among medically ill patients resulted in significantly more—not less—depressive symptoms.
Lower functional hippocampal redundancy in mild cognitive impairment
Authors: Langella Stephanie , Sadiq Muhammad Usman , Mucha Peter J. , Giovanello Kelly S. , Dayan Eran ,   for the Alzheimer’s Disease Neuroimaging Initiative
Published: January 2021

AbstractWith an increasing prevalence of mild cognitive impairment (MCI) and Alzheimer’s disease (AD) in response to an aging population, it is critical to identify and understand neuroprotective mechanisms against cognitive decline. One potential mechanism is redundancy: the existence of duplicate elements within a system that provide alternative functionality in case of failure. As the hippocampus is one of the earliest sites affected by AD pathology, we hypothesized that functional hippocampal redundancy is protective against cognitive decline. We compared hippocampal functional redundancy derived from resting-state functional MRI networks in cognitively normal older adults, with individuals with early and late MCI, as well as the relationship between redundancy and cognition. Posterior hippocampal redundancy was reduced between cognitively normal and MCI groups, plateauing across early and late MCI. Higher hippocampal redundancy was related to better memory performance only for cognitively normal individuals. Critically, functional hippocampal redundancy did not come at the expense of network efficiency. Our results provide support that hippocampal redundancy protects against cognitive decline in aging.
The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor
Authors: Dingsdale Hayley , Nan Xinsheng , Garay Samantha M. , Mueller Annett , Sumption Lorna A. , Chacón-Fernández Pedro , Martinez-Garay Isabel , Ghevaert Cedric , Barde Yves-Alain , John Rosalind M. 
Published: January 2021

AbstractBrain-derived neurotrophic factor (BDNF) plays crucial roles in brain function. Numerous studies report alterations in BDNF levels in human serum in various neurological conditions, including mood disorders such as depression. However, little is known about BDNF levels in the blood during pregnancy. We asked whether maternal depression and/or anxiety during pregnancy were associated with altered serum BDNF levels in mothers (n = 251) and their new-born infants (n = 212). As prenatal exposure to maternal mood disorders significantly increases the risk of neurological conditions in later life, we also examined the possibility of placental BDNF transfer by developing a new mouse model. We found no association between maternal symptoms of depression and either maternal or infant cord blood serum BDNF. However, maternal symptoms of anxiety correlated with significantly raised maternal serum BDNF exclusively in mothers of boys (r = 0.281; P = 0.005; n = 99). Serum BDNF was significantly lower in male infants than female infants but neither correlated with maternal anxiety symptoms. Consistent with this observation, we found no evidence for BDNF transfer across the placenta. We conclude that the placenta protects the developing fetus from maternal changes in serum BDNF that could otherwise have adverse consequences for fetal development.
MEDAG enhances breast cancer progression and reduces epirubicin sensitivity through the AKT/AMPK/mTOR pathway
Authors: Li Zhiyu , Li Chenyuan , Wu Qi , Tu Yi , Wang Changhua , Yu Xin , Li Bei , Wang Zhong , Sun Si , Sun Shengrong 
Published: January 2021

AbstractBreast cancer (BC) is the most common malignancy among women. Mesenteric estrogen-dependent adipogenesis gene (MEDAG) was first reported as a novel adipogenic gene, and its involvement and mechanism in visceral adiposity were analyzed. However, the role of MEDAG in BC is unclear. The biological roles and corresponding mechanisms were investigated in vitro and in vivo. We found that MEDAG was highly expressed in BC samples and that a high MEDAG expression was correlated with clinicopathological characteristics and poor survival in BC patients. MEDAG knockdown inhibited cell proliferation, invasion, and migration; triggered epithelial-to-mesenchymal transition (EMT); and enhanced epirubicin sensitivity in vitro. The opposite results were observed in MEDAG-overexpressing cells. The inhibition of MEDAG suppressed tumor growth and metastasis in vivo. Mechanistically, MEDAG knockdown led to decreased phosphorylation levels of AKT, increased levels of p-AMPK, and reduced levels of p-mTOR, while the overexpression of MEDAG had the opposite effects. Moreover, the activation of p-AKT and inhibition of p-AMPK restored the effect of MEDAG on EMT and chemosensitivity in BC cell lines, indicating that MEDAG functions as an oncogene by regulating the AKT/AMPK/mTOR pathway. MEDAG regulates BC progression and EMT via the AKT/AMPK/mTOR pathway and reduces chemosensitivity in BC cells. Therefore, MEDAG is a promising target for BC.
Wnt5a promotes renal tubular inflammation in diabetic nephropathy by binding to CD146 through noncanonical Wnt signaling
Authors: Li Xiaomei , Wen Jiejun , Dong Yang , Zhang Qunzi , Guan Jian , Liu Feng , Zhou Ting , Li Ze , Fan Ying , Wang Niansong 
Published: January 2021

AbstractImmune and inflammatory factors have emerged as key pathophysiological mechanisms in the progression of diabetic renal injury. Noncanonical Wnt5a signaling plays an essential role in obesity- or diabetes-induced metabolic dysfunction and inflammation, but its explicit molecular mechanisms and biological function in diabetic nephropathy (DN) remain unknown. In this study, we found that the expression of Wnt5a and CD146 in the kidney and the level of soluble form of CD146 (sCD146) in serum and urine samples were upregulated in DN patients compared to controls, and this alteration was correlated with the inflammatory process and progression of renal impairment. Blocking the activation of Wnt5a signaling with the Wnt5a antagonist Box5 prevented JNK phosphorylation and high glucose-induced inflammatory responses in db/db mice and high glucose-treated HK-2 cells. Similar effects were observed by silencing Wnt5a with small-interfering RNA (siRNA) in cultured HK-2 cells. Knockdown of CD146 blocked Wnt5a-induced expression of proinflammatory cytokines and activation of JNK, which suggests that CD146 is essential for the activation of the Wnt5a pathway. Finally, we confirmed that Wnt5a directly interacted with CD146 to activate noncanonical Wnt signaling in HK-2 cells. Taken together, our findings suggest that by directly binding to CD146, Wnt5a-induced noncanonical signaling is a contributing mechanism for renal tubular inflammation in diabetic nephropathy. The concentration of sCD146 in serum and urine could be a potential biomarker to predict renal outcomes in DN patients.
M2-like macrophages exert hepatoprotection in acute-on-chronic liver failure through inhibiting necroptosis-S100A9-necroinflammation axis
Authors: Bai Li , Kong Ming , Duan Zhongping , Liu Shuang , Zheng Sujun , Chen Yu 
Published: January 2021

AbstractNecroptosis has emerged as a novel and crucial player in acute and chronic liver diseases. Necroptotic cells lead to the release of DAMPs including S100A9, followed by the development of necroinflammation. We previously have documented the beneficial hepatoprotection conferred by M2-like macrophages in acute-on-chronic liver failure (ACLF) in vitro and in vivo, namely, M2-like macrophages protect hepatocytes against apoptosis. Herein, we integrated necroptosis, S100A9, and necroinflammation into this hepatoprotection, and hypothesized M2-like macrophages exert a hepatoprotective effect through inhibiting necroptosis-S100A9-necroinflammation axis. To testify this hypothesis, control mice were pre-treated with necroptosis or S100A9 inhibitors followed by D-GalN/LPS challenge. The extent of liver injury and M1/M2 macrophage activation was assessed. Necroptosis signaling and S100A9 expression were analysed and compared in control and fibrotic mice with or without acute insult. To document the pivotal role of M2-like macrophages in necroptosis and S100A9 inhibition, loss-of-function and gain-of-function experiments were performed. In addition, necroinflammation and its dependence on necroptosis and S100A9 were analysed. Moreover, the inhibitory effects of M2-like macrophages on necroinflammation were investigated in vivo and in vitro. We found that: firstly, the inhibition of necroptosis signaling and S100A9 expression alleviated D-GalN/LPS-induced hepatic damage, which was accompanied by M2-like macrophage activation; secondly, fibrosis inhibited necroptosis signaling and S100A9 expression, which could be attributed to M2-like macrophage activation; thirdly, S100A9 may function as a downstream player of necroptosis signaling; fourthly, fibrosis suppressed necroptosis- and S100A9-dependent necroinflammation; and finally, M2-like macrophages inhibited NLRP3 inflammasome activation and resultant necroinflammation via IL-10. Therefore, M2-like macrophages exert a beneficial hepatoprotection by inhibiting necroptosis-S100A9-necroinflammation axis in ACLF. Our findings provide novel insight for treating ACLF patients by specially targeting this signaling axis.
miR-541-3p enhances the radiosensitivity of prostate cancer cells by inhibiting HSP27 expression and downregulating β-catenin
Authors: He Zhenhua , Shen Fuhui , Qi Ping , Zhai Zhenxing , Wang Zhiping 
Published: January 2021

AbstractHeat shock protein 27 (HSP27), a regulator of cell survival, can enhance the resistance of cancer cells to radiotherapy. As microRNA-541-3p (miR-541-3p) was recently predicted to be a putative upstream modulator of HSP27, the present study was designed to investigate the function and mechanism underlying how miR-541-3p modulates the radiosensitivity of prostate cancer (PCa) cells by regulating HSP27. Through quantitative PCR, miR-541-3p was determined to be poorly expressed in PCa tissues relative to normal controls, whereas its expression was enhanced after radiotherapy. Consistently, miR-541-3p expression levels in PCa cells were elevated after radiation. Cell viability and proliferation and apoptosis under radiation were subsequently evaluated in response to loss-of-function of miR-541-3p. It was found that inhibition of miR-541-3p facilitated the viability and proliferation of PCa cells and promoted their apoptosis post radiation, hence reducing the radiosensitivity of LNCaP cells. Dual-luciferase reporter assay identified that miR-541-3p negatively regulated the HSP27 mRNA expression by targeting its 3′-UTR. Meanwhile, miR-541-3p overexpression inhibited the β-catenin expression by targeting HSP27. Furthermore, HSP27 or β-catenin overexpression was noted to significantly reverse the miR-541-3p-mediated changes in the biological functions of PCa cells post radiation, suggesting that HSP27-dependent activation of β-catenin might be the mechanism responsible for the promotive effect of miR-541-3p on radiosensitivity. Collectively, this study suggests that miR-541-3p specifically inhibits the HSP27 expression and downregulates β-catenin, thereby enhancing the radiosensitivity of PCa cells. Our findings highlight the underlying mechanism of the miR-541-3p/HSP27/Wnt/β-catenin axis regarding radiotherapy for PCa.