bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence that a novel transdiagnostic eating disorder treatment reduces reward region response to the thin beauty ideal and high-calorie binge foods
Authors: Stice Eric , Yokum Sonja , Rohde Paul , Gau Jeff , Shaw Heather 
Published: October 2021

AbstractBackgroundFindings from brain imaging studies with small samples can show limited reproducibility. Thus, we tested whether the evidence that a transdiagnostic eating disorder treatment reduces responsivity of brain valuation regions to thin models and high-calorie binge foods, the intervention targets, from a smaller earlier trial emerged when we recruited additional participants.MethodsWomen with DSM-5 eating disorders (N = 138) were randomized to the dissonance-based body project treatment (BPT) or a waitlist control condition and completed functional magnetic resonance imaging (fMRI) scans assessing neural response to thin models and high-calorie foods at pretest and posttest.ResultsBPT v. control participants showed significantly greater reductions in responsivity of regions implicated in reward valuation (caudate) and attentional motivation (precuneus) to thin v. average-weight models, echoing findings from the smaller sample. Data from this larger sample also provided novel evidence that BPT v. control participants showed greater reductions in responsivity of regions implicated in reward valuation (ventrolateral prefrontal cortex) and food craving (hippocampus) to high-calorie binge foods v. low-calorie foods, as well as significantly greater reductions in eating disorder symptoms, abstinence from binge eating and purging behaviors, palatability ratings for high calorie foods, monetary value for high-calorie binge foods, and significantly greater increases in attractiveness ratings of average weight models.ConclusionsResults from this larger sample provide evidence that BPT reduces valuation of the thin ideal and high-calorie binge foods, the intervention targets, per objective brain imaging data, and produces clinically meaningful reductions in eating pathology.
Dynamics of diurnal cortisol and alpha-amylase secretion and their associations with PTSD onset in recent interpersonal trauma survivors
Authors: Kinney Kerry L. , Rao Uma , Bailey Brooklynn , Hellman Natalie , Kelly Chris , McAfee Nicholas W. , Morris Matthew C. 
Published: October 2021

AbstractBackgroundDysfunction in major stress response systems during the acute aftermath of trauma may contribute to risk for developing posttraumatic stress disorder (PTSD). The current study investigated how PTSD diagnosis and symptom severity, depressive symptoms, and childhood trauma uniquely relate to diurnal neuroendocrine secretion (cortisol and alpha-amylase rhythms) in women who recently experienced interpersonal trauma compared to non-traumatized controls (NTCs).MethodUsing a longitudinal design, we examined diurnal cortisol and alpha-amylase rhythms in 98 young women (n= 57 exposed to recent interpersonal trauma,n= 41 NTCs). Participants provided saliva samples and completed symptom measures at baseline and 1-, 3-, and 6-month follow-up.ResultsMultilevel models (MLMs) revealed lower waking cortisol predicted the development of PTSD in trauma survivors and distinguished at-risk women from NTCs. Women with greater childhood trauma exposure exhibited flatter diurnal cortisol slopes. Among trauma-exposed individuals, lower waking cortisol levels were associated with higher concurrent PTSD symptom severity. Regarding alpha-amylase, MLMs revealed women with greater childhood trauma exposure exhibited higher waking alpha-amylase and slower diurnal alpha-amylase increase.ConclusionsResults suggest lower waking cortisol in the acute aftermath of trauma may be implicated in PTSD onset and maintenance. Findings also suggest childhood trauma may predict a different pattern of dysfunction in stress response systems following subsequent trauma exposure than the stress system dynamics associated with PTSD risk; childhood trauma appears to be associated with flattened diurnal cortisol and alpha-amylase slopes, as well as higher waking alpha-amylase.
Disclosure versus recognition: the value relevance of pensions
Authors: Larcher Luca 
Published: October 2021

AbstractThis paper compares how pension obligations impact the market value of United States corporations under two accounting regimes. Using a sample of firms that disclosed pension liabilities under Statement of Financial Accounting Standards (SFAS) No. 87 from 2001 to 2005 and recognized them under SFAS No. 158 from 2006 to 2014, I find that equity market participants take into account the net position of the pension fund only if it is recognized on the sponsor's balance sheet, thus mispricing the pension deficit/surplus under the disclosure regime. I also provide evidence suggesting that investors' perception of pension deficits/surpluses changed with the introduction of SFAS No. 158 in 2006.
One country, two systems: evidence on retirement patterns in China
Authors: Giles John , Lei Xiaoyan , Wang Gewei , Wang Yafeng , Zhao Yaohui 
Published: October 2021

AbstractThis paper documents the patterns and correlates of retirement in China using a nationally representative survey, the China Health and Retirement Longitudinal Study. After documenting stark differences in retirement ages between urban and rural residents, the paper shows that China's urban residents retire earlier than workers in many Organization for Economic Co-operation and Development countries and that rural residents continue to work until advanced ages. Differences in access to generous pensions and economic resources explain much of the urban–rural difference in retirement rates. The paper suggests that reducing disincentives created by China's Urban Employee Pension system, improving health status, providing childcare and elder care support may all facilitate longer working lives. Given spouse preferences for joint retirement, creating incentives for women to retire later may facilitate longer working lives for both men and women.
Storage duration increases oxidation products in peanut seeds
Authors: Tonnis Brandon , Wang Ming Li , Huang Edward , Bhattarai Uttam , Tallury Shyam 
Published: October 2021

AbstractSeeds kept in long-term storage are essential for maintaining genetic resources of crops and other plant materials in seed banks and national germplasm systems. But seeds undergo chemical changes over time as part of the ageing process that result in reduced germination rates and seedling normalcy. For example, oilseed crops such as peanuts are particularly vulnerable to oxidation and rancidification due to their high oil content. To test the effect of storage time on seed oil in peanuts, we grew different accessions and harvested fresh seeds to compare the oil composition of new seeds with seeds aged in storage for varying lengths of time. Out of the nine fatty acids detected and measured by gas chromatography, five including oleic, gadoleic, behenic, lignoceric and cerotic acids differed significantly between new and old seeds. Additionally, old seeds accumulated up to four oxidation products together averaging about 1% of the total oil composition. The concentration of these oxidation products was positively correlated with the age of the seeds, increasing linearly up to more than 6% of the total in the oldest seeds. The presence and concentration of oxidation products measured using simple chromatography techniques can be used as an initial indication of quality and viability in older seed inventories stored in germplasm repositories.
Continental Tectonics Inferred From High‐Resolution Imaging of the Mantle Beneath the United States, Through the Combination of USArray Data Types
Authors: Bedle Heather , Lou Xiaoting , van der Lee Suzan 
Published: October 2021

AbstractA comprehensive North American upper mantle seismic‐tomographic model, NA13, was inferred from a combination of several decades of seismic data from early North American seismic networks and USArray data. This data‐driven modeling inverted a combination of regional waveform fits, teleseismic S delay times, and point constraints on Moho depths. The joint inversion model combines the contrasting and overlapping resolving power of the different data sets, and demonstrates enhanced resolution over regional models created with a single geophysical data set. Resolution in the upper mantle is achieved on the scale of ∼100 km, although travel time delay studies suggest that anomalies in parts of the western United States are smaller. In NA13, velocities beneath the Yellowstone plume are low enough to require the presence of partial melt. NA13 also models a variety of smaller scale velocity variations beneath the Central and Eastern United States that reveal remnant velocity anomalies related to lithospheric variations in the upper mantle between Proterozoic units.
Direct Radiative Effects in Haboobs
Authors: Bukowski J. , van den Heever S. C. 
Published: October 2021

AbstractConvective dust storms, or haboobs, form when strong surface winds loft loose soils in convective storm outflow boundaries. Haboobs are a public safety hazard and can cause a near instantaneous loss of visibility, inimical air quality, and contribute significantly to regional dust and radiation budgets. Nevertheless, reliable predictions of convective dust events are inhibited by a lack of understanding regarding the complex and non‐linear interactions between density currents, or convective cold pools, and dust radiative effects. In this study, the Weather Research and Forecasting model coupled with Chemistry (WRF‐Chem) is utilized to simulate the effect dust radiation interactions have on a long‐lived haboob case study that spans three distinct radiative regimes: day (high shortwave), evening (low shortwave), and night [longwave (LW) only]. A sophisticated algorithm is used to track and identify the numerous convective old pool boundaries in the simulations and assemble statistics that represent the impact of dust radiative effects. To first order, dust scattering of shortwave radiation in the day leads to a colder, dustier, and faster moving convective cold pool. In the transition period of early evening, the shortwave effects diminish while LW dust absorption leads to warmer, slower density currents that loft less dust as they propagate. At night, the haboob is again warmer due to dust absorption, but gustier in the more stable nocturnal surface layer, leading to enhanced dust emissions.
Cardiovascular mortality risk in young adults with isolated systolic hypertension: findings from population-based MONICA/KORA cohort study
Authors: Atasoy Seryan , Middeke Martin , Johar Hamimatunnisa , Peters Annette , Heier Margit , Ladwig Karl-Heinz 
Published: October 2021

AbstractThe clinical significance of isolated systolic hypertension in young adults (ISHY) remains a topic of debate due to evidence ISHY could be a spurious condition resulting from exageratted pulse pressure amplification in “young tall men with elastic arteries”. Hence, we aimed to investigate whether ISHY is associated with an increased risk of cardivascular (CVD) mortality in a sample of 5597 young adults (49.8% men, 50.2% women) between 25 and 45 years old from the prospective population-based MONICA/KORA cohort. ISHY was prevalent in 5.2% of the population, affecting mostly men (73.1%), and associated with increased smoking, obesity, and hypercholesterolemia in comparison to participants with normal blood pressure (BP). Within a follow-up period of 25.3 years (SD ± 5.2; 141,768 person–years), 133(2.4%) CVD mortality cases were observed. Participants with ISHY had a hazard ratio (HR) of 1.89(1.01–3.53, p < 0.05) times higher risk of CVD mortality than participants with normal BP, even following adjustment for CVD risk factors. However, adjustment for antihypertensive medication (HR 0.46; 0.26–0.81, p < 0.001) and increasing height (HR 0.96; 0.93–0.99, p < 0.05) revealed independently protective effects against CVD mortality, suggesting that although ISHY is associated with an increased risk of CVD mortality, the protective effects of increasing height or antihypertensive medication should be considered in treatment rationale.
A triple-network organization for the mouse brain
Authors: Mandino Francesca , Vrooman Roël M. , Foo Heidi E. , Yeow Ling Yun , Bolton Thomas A. W. , Salvan Piergiorgio , Teoh Chai Lean , Lee Chun Yao , Beauchamp Antoine , Luo Sarah , Bi Renzhe , Zhang Jiayi , Lim Guan Hui Tricia , Low Nathaniel , Sallet Jerome , Gigg John , Lerch Jason P. , Mars Rogier B. , Olivo Malini , Fu Yu , Grandjean Joanes 
Published: October 2021

AbstractThe triple-network model of psychopathology is a framework to explain the functional and structural neuroimaging phenotypes of psychiatric and neurological disorders. It describes the interactions within and between three distributed networks: the salience, default-mode, and central executive networks. These have been associated with brain disorder traits in patients. Homologous networks have been proposed in animal models, but their integration into a triple-network organization has not yet been determined. Using resting-state datasets, we demonstrate conserved spatio-temporal properties between triple-network elements in human, macaque, and mouse. The model predictions were also shown to apply in a mouse model for depression. To validate spatial homologies, we developed a data-driven approach to convert mouse brain maps into human standard coordinates. Finally, using high-resolution viral tracers in the mouse, we refined an anatomical model for these networks and validated this using optogenetics in mice and tractography in humans. Unexpectedly, we find serotonin involvement within the salience rather than the default-mode network. Our results support the existence of a triple-network system in the mouse that shares properties with that of humans along several dimensions, including a disease condition. Finally, we demonstrate a method to humanize mouse brain networks that opens doors to fully data-driven trans-species comparisons.
O-GlcNAc modified-TIP60/KAT5 is required for PCK1 deficiency-induced HCC metastasis
Authors: Liu Rui , Gou Dongmei , Xiang Jin , Pan Xuanming , Gao Qingzhu , Zhou Peng , Liu Yi , Hu Jie , Wang Kai , Tang Ni 
Published: October 2021

AbstractAberrant glucose metabolism and elevated O-linked β-N-acetylglucosamine modification (O-GlcNAcylation) are hallmarks of hepatocellular carcinoma (HCC). Loss of phosphoenolpyruvate carboxykinase 1 (PCK1), the major rate-limiting enzyme of hepatic gluconeogenesis, increases hexosamine biosynthetic pathway (HBP)-mediated protein O-GlcNAcylation in hepatoma cell and promotes cell growth and proliferation. However, whether PCK1 deficiency and hyper O-GlcNAcylation can induce HCC metastasis is largely unknown. Here, gain- and loss-of-function studies demonstrate that PCK1 suppresses HCC metastasis in vitro and in vivo. Specifically, lysine acetyltransferase 5 (KAT5), belonging to the MYST family of histone acetyltransferases (HAT), is highly modified by O-GlcNAcylation in PCK1 knockout hepatoma cells. Mechanistically, PCK1 depletion suppressed KAT5 ubiquitination by increasing its O-GlcNAcylation, thereby stabilizing KAT5. KAT5 O-GlcNAcylation epigenetically activates TWIST1 expression via histone H4 acetylation, and enhances MMP9 and MMP14 expression via c-Myc acetylation, thus promoting epithelial-mesenchymal transition (EMT) in HCC. In addition, targeting HBP-mediated O-GlcNAcylation of KAT5 inhibits lung metastasis of HCC in hepatospecific Pck1-deletion mice. Collectively, our findings demonstrate that PCK1 depletion increases O-GlcNAcylation of KAT5, epigenetically induces TWIST1 expression and promotes HCC metastasis, and link metabolic enzyme, post-translational modification (PTM) with epigenetic regulation.
Metformin alleviates inflammation through suppressing FASN-dependent palmitoylation of Akt
Authors: Xiong Wenfang , Sun Kuo-Yang , Zhu Yan , Zhang Xiaoqi , Zhou Yi-Hua , Zou Xiaoping 
Published: October 2021

AbstractMetformin, traditionally regarded as a hypoglycemic drug, has been studied in other various fields including inflammation. The specific mechanism of metformin’s effect on immune cells remains unclear. Herein, it is verified that LPS-induced macrophages are characterized by enhanced endogenous fatty acid synthesis and the inhibition of fatty acid synthase (FASN) downregulates proinflammatory responses. We further show that metformin could suppress such elevation of FASN as well as proinflammatory activation in macrophages. In vivo, metformin treatment ameliorates dextran sulfate sodium (DSS)-induced colitis through impairing proinflammatory activation of colonic lamina propria mononuclear cells (LPMCs). The reduction of FASN by metformin hinders Akt palmitoylation, which further disturbs Akt membrane attachment and its phosphorylation. Metformin-mediated suppression of FASN/Akt pathway and its downstream MAPK signaling contributes to its anti-inflammatory role in macrophages. From the perspective of immunometabolism, our work points towards metformin utilization as an effective and potential intervention against macrophages-involved inflammatory diseases.
The Hh pathway promotes cell apoptosis through Ci-Rdx-Diap1 axis
Authors: Liu Bin , Ding Yan , Sun Bing , Liu Qingxin , Zhou Zizhang , Zhan Meixiao 
Published: October 2021

AbstractApoptosis is a strictly coordinated process to eliminate superfluous or damaged cells, and its deregulation leads to birth defects and various human diseases. The regulatory mechanism underlying apoptosis still remains incompletely understood. To identify novel components in apoptosis, we carry out a modifier screen and find that the Hh pathway aggravates Hid-induced apoptosis. In addition, we reveal that the Hh pathway triggers apoptosis through its transcriptional target gene rdx, which encodes an E3 ubiquitin ligase. Rdx physically binds Diap1 to promote its K63-linked polyubiquitination, culminating in attenuating Diap1−Dronc interaction without affecting Diap1 stability. Taken together, our findings unexpectedly uncover the oncogenic Hh pathway is able to promote apoptosis through Ci-Rdx-Diap1 module, raising a concern to choose Hh pathway inhibitors as anti-tumor drugs.
The selective degradation of sirtuins via macroautophagy in the MPP+ model of Parkinson’s disease is promoted by conserved oxidation sites
Authors: Baeken Marius W. , Schwarz Mario , Kern Andreas , Moosmann Bernd , Hajieva Parvana , Behl Christian 
Published: October 2021

AbstractThe sirtuin (SIRT) protein family has been of major research interest over the last decades because of their involvement in aging, cancer, and cell death. SIRTs have been implicated in gene and metabolic regulation through their capacity to remove acyl groups from lysine residues in proteins in an NAD+-dependent manner, which may alter individual protein properties as well as the histone–DNA interaction. Since SIRTs regulate a wide range of different signaling cascades, a fine-tuned homeostasis of these proteins is imperative to guarantee the function and survival of the cell. So far, however, how exactly this homeostasis is established has remained unknown. Here, we provide evidence that neuronal SIRT degradation in Parkinson’s disease (PD) models is executed by autophagy rather than the proteasome. In neuronal Lund human mesencephalic (LUHMES) cells, all seven SIRTs were substrates for autophagy and showed an accelerated autophagy-dependent degradation upon 1-methyl-4-phenylpyridinium (MPP+) mediated oxidative insults in vitro, whereas the proteasome did not contribute to the removal of oxidized SIRTs. Through blockade of endogenous H2O2 generation and supplementation with the selective radical scavenger phenothiazine (PHT), we could identify H2O2-derived species as the responsible SIRT-oxidizing agents. Analysis of all human SIRTs suggested a conserved regulatory motif based on cysteine oxidation, which may have triggered their degradation via autophagy. High amounts of H2O2, however, rapidly carbonylated selectively SIRT2, SIRT6, and SIRT7, which were found to accumulate carbonylation-prone amino acids. Our data may help in finding new strategies to maintain and modify SIRT bioavailability in neurodegenerative disorders.
Downregulation of phosphoglycerate mutase 5 improves microglial inflammasome activation after traumatic brain injury
Authors: Chen Yuhua , Gong Kai , Guo Limin , Zhang Bingchang , Chen Sifang , Li Zhangyu , Quanhua Xu , Liu Wei , Wang Zhanxiang 
Published: October 2021

AbstractTraumatic brain injury (TBI) is considered as the most common cause of disability and death, and therefore an effective intervention of cascade pathology of secondary brain injury promptly can be a potential therapeutic direction for TBI prognosis. Further study of the physiological mechanism of TBI is urgent and important. Phosphoglycerate mutase 5 (Pgam5), a mitochondrial protein, mediate mitochondrial homeostasis, cellular senescence, and necroptosis. This study evaluated the effects of Pgam5 on neurological deficits and neuroinflammation of controlled cortical impact-induced TBI mouse model in vivo and LPS + ATP-induced microglia model in vitro. Pgam5 was overexpressed post-TBI. Pgam5 depletion reduced pyroptosis-related molecules and improved microglia activation, neuron damage, tissue lesion, and neurological dysfunctions in TBI mice. RNA-seq analysis and molecular biology experiments demonstrated that Pgam5 might regulate inflammatory responses by affecting the post-translational modification and protein expression of related genes, including Nlrp3, caspase1, Gsdmd, and Il-1β. In microglia, Pgam5-sh abrogated LPS + ATP-induced Il-1β secretion through Asc oligomerization-mediated caspase-1 activation, which was independent of Rip3. The data demonstrate the critical role Pgam5 plays in nerve injury in the progression of TBI, which regulates Asc polymerization and subsequently caspase1 activation, and thus reveals a fundamental mechanism linking microglial inflammasome activation to Asc/caspase1-generated Il-1β-mediated neuroinflammation. Thus, our data indicate Pgam5 worsens physiological and neurological outcomes post-TBI, which may be a potential therapeutic target to improve neuroinflammation after TBI.
Structures of active melanocortin-4 receptor–Gs-protein complexes with NDP-α-MSH and setmelanotide
Authors: Heyder Nicolas A. , Kleinau Gunnar , Speck David , Schmidt Andrea , Paisdzior Sarah , Szczepek Michal , Bauer Brian , Koch Anja , Gallandi Monique , Kwiatkowski Dennis , Bürger Jörg , Mielke Thorsten , Beck-Sickinger Annette G. , Hildebrand Peter W. , Spahn Christian M. T. , Hilger Daniel , Schacherl Magdalena , Biebermann Heike , Hilal Tarek , Kühnen Peter , Kobilka Brian K. , Scheerer Patrick 
Published: October 2021

AbstractThe melanocortin-4 receptor (MC4R), a hypothalamic master regulator of energy homeostasis and appetite, is a class A G-protein-coupled receptor and a prime target for the pharmacological treatment of obesity. Here, we present cryo-electron microscopy structures of MC4R–Gs-protein complexes with two drugs recently approved by the FDA, the peptide agonists NDP-α-MSH and setmelanotide, with 2.9 Å and 2.6 Å resolution. Together with signaling data from structure-derived MC4R mutants, the complex structures reveal the agonist-induced origin of transmembrane helix (TM) 6-regulated receptor activation. The ligand-binding modes of NDP-α-MSH, a high-affinity linear variant of the endogenous agonist α-MSH, and setmelanotide, a cyclic anti-obesity drug with biased signaling toward Gq/11, underline the key role of TM3 in ligand-specific interactions and of calcium ion as a ligand-adaptable cofactor. The agonist-specific TM3 interplay subsequently impacts receptor–Gs-protein interfaces at intracellular loop 2, which also regulates the G-protein coupling profile of this promiscuous receptor. Finally, our structures reveal mechanistic details of MC4R activation/inhibition, and provide important insights into the regulation of the receptor signaling profile which will facilitate the development of tailored anti-obesity drugs.