bluuebunny/crossref_metadata_2025_split huggingface dataset:
A twin‐screw extruder for oil extraction: I. Direct expression of oleic sunflower seeds
Authors: Dufaure Corinne , Leyris Juliette , Rigal Luc , Mouloungui Zéphirin 
Published: January 2018

AbstractLipids are traditionally removed from seeds by mechanical crushing and solvent extraction. During the mechanical crushing process the oilseed is cleaned, cracked, flaked, and cooked before entering a mechanical screw press. Seventy‐five percent of the oil of sunflower seeds can be extracted by crushing, and the fatty cake then contains about 15% of oil. The oil levels remaining in the cake can be reduced to less than 2% by solvent extraction. However, the crude oil has to be refined as it contains many impurities and approximately 600 ppm phosphorus. A new process, in which sunflower seeds are pressed in a twin‐screw extruder, is examined here. The screw profile was first optimized. Oleic sunflower seeds were crushed and 80% of the oil was removed. The resultant oil was of good quality, with acid numbers below 2 mg KOH/g of oil and total phosphorus contents of about 100 ppm. The influence of pressing temperature and of fresh seed moisture content was determined. High pressing temperature and low moisture content improved oil extraction. The quality of the meal was examined through the solubilization of its proteins in alkaline water at 50°C. The fatty meal proteins remained quite soluble, and therefore one can assume that they were still relatively close to their native conformation. The pressing of oleaginous material in a twin‐screw extruder provides a new option to traditional processes.
A modified VERI‐FRY® quick test for measuring total polar compounds in deep‐frying oils
Authors: Xu Xin‐Qing 
Published: January 2018

AbstractThe AOCS official method for the determination of total polar compounds in deep‐frying oils is often used to estimate frying oil degradation. It can be accurate and reliable, but with sacrifices of time and expense. The TPM VERI‐FRY® PRO (Libra Technologies, Inc., Metuchen, NJ) quick test provides a quick and easy way to measure polar compounds in frying oils. The modified quick test measured at 490 nm has a good correlation with the AOCS official method (r=0.975, P<0.001) and provides a good estimate of polar compound accumulation in oils over 80 h of deep‐frying. Using the quick test to measure polar compounds is fast, convenient, economical and reliable.
The association and dose–response relationship between dietary intake of α-linolenic acid and risk of CHD: a systematic review and meta-analysis of cohort studies
Authors: Wei Jingkai , Hou Ruixue , Xi Yuzhi , Kowalski Alysse , Wang Tiansheng , Yu Zhi , Hu Yirui , Chandrasekar Eeshwar K. , Sun Hao , Ali Mohammed K. 
Published: January 2018

AbstractPrevious studies show inconsistent associations between α-linolenic acid (ALA) and risk of CHD. We aimed to examine an aggregate association between ALA intake and risk of CHD, and assess for any dose–response relationship. We searched the PubMed, EMBASE and Web of Science databases for prospective cohort studies examining associations between ALA intake and CHD, including composite CHD and fatal CHD. Data were pooled using random-effects meta-analysis models, comparing the highest category of ALA intake with the lowest across studies. Subgroup analysis was conducted based on study design, geographic region, age and sex. For dose–response analyses, we used two-stage random-effects dose–response models. In all, fourteen studies of thirteen cohorts were identified and included in the meta-analysis. The pooled results showed that higher ALA intake was associated with modest reduced risk of composite CHD (risk ratios (RR)=0·91; 95 % CI 0·85, 0·97) and fatal CHD (RR=0·85; 95 % CI 0·75, 0·96). The analysis showed a J-shaped relationship between ALA intake and relative risk of composite CHD (χ2=21·95, P<0·001). Compared with people without ALA intake, only people with ALA intake <1·4 g/d showed reduced risk of composite CHD. ALA intake was linearly associated with fatal CHD – every 1 g/d increase in ALA intake was associated with a 12 % decrease in fatal CHD risk (95 % CI −0·21, −0·04). Though a higher dietary ALA intake was associated with reduced risk of composite and fatal CHD, the excess composite CHD risk at higher ALA intakes warrants further investigation, especially through randomised controlled trials.
Episodic memory isn't essentially autonoetic
Authors: Carruthers Peter 
Published: January 2018

AbstractI argue that the function attributed to episodic memory by Mahr & Csibra (M&C) – that is, grounding one's claims to epistemic authority over past events – fails to support the essentially autonoetic character of such memories. I suggest, in contrast, that episodic event memories are sometimes purely first order, sometimes autonoetic, depending on relevance in the context.
Episodic memory is as much about communicating as it is about relating to others
Authors: Coman Alin 
Published: January 2018

AbstractMahr & Csibra (M&C) provide extensive evidence for the communicative function of episodic memory, suggesting that the malleability of human memory is in large part due to its communicative dimension. I argue that emphasizing the relational motivations involved in communication provides a more proximal explanation for why our memories are as malleable.
Episodic memory and consciousness in antisocial personality disorder and conduct disorder
Authors: Fabbro Franco , Crescentini Cristiano 
Published: January 2018

AbstractEpisodic memory is one of the most significant sources of information of humans. It entails cooperative and linguistic skills and, as Mahr & Csibra (M&C) note, the capacity to ground veridical beliefs about the past. In some psychiatric disorders (antisocial personality disorder and conduct disorder), it was found that the habit of lying is associated with episodic memory and consciousness deficits.
“Truth be told” – Semantic memory as the scaffold for veridical communication
Authors: Hayes Brett K. , Ramanan Siddharth , Irish Muireann 
Published: January 2018

AbstractTheoretical accounts placing episodic memory as central to constructive and communicative functions neglect the role of semantic memory. We argue that the decontextualized nature of semantic schemas largely supersedes the computational bottleneck and error-prone nature of episodic memory. Rather, neuroimaging and neuropsychological evidence of episodic-semantic interactions suggest that an integrative framework more accurately captures the mechanisms underpinning social communication.
More to episodic memory than epistemic assertion: The role of social bonds and interpersonal connection
Authors: Hirst William , Echterhoff Gerald 
Published: January 2018

AbstractRemembering is dynamically entangled in conversations. The communicative function of episodic memory can be epistemic, as suggested by Mahr & Csibra (M&C). However, remembering can have genuinely social functions, specifically, the creation or consolidation of interpersonal relationships. Autonoesis, a distinct feature of episodic memory, is more likely to have evolved in the service of social binding than of epistemic assertiveness.
Carving event and episodic memory at their joints
Authors: Keven Nazim 
Published: January 2018

AbstractMahr & Csibra (M&C) argue that event and episodic memories share the same scenario construction process. I think this way of carving up the distinction throws the baby out with the bathwater. If there is a substantive difference between event and episodic memory, it is based on a difference in the construction process and how they are organized, respectively.
Episodic memory solves both social and nonsocial problems, and evolved to fulfill many different functions
Authors: Mar Raymond A. , Spreng R. Nathan 
Published: January 2018

AbstractThe episodic memory system is flexible and complex, and likely evolved in response to a wide range of survival-relevant problems in our evolutionary past, both social and nonsocial. Episodic memory allows us to recollect and infer details that may have seemed trivial on encoding, but are now known to be relevant. This memory aids humans in navigating their uncertain environment.
Morgan's canon is not evidence
Authors: Samuel Steven , Clayton Nicola 
Published: January 2018

AbstractMahr & Csibra's (M&C's) account of the communicative function of episodic memory relies more heavily on the case against episodic memory in nonhumans than their description suggests. Although the communicative function of episodic memory may be accurate as it pertains to human behaviour, we question whether Morgan's canon is a suitable foundation on which to build theories of supposedly human-specific traits.
What is it to remember?
Authors: Mahr Johannes B. , Csibra Gergely 
Published: January 2018

AbstractIn response to the commentaries, we clarify and defend our characterization of both the nature and function of episodic memory. Regarding the nature of episodic memory, we extend the distinction between event and episodic memory and discuss the relational role of episodic memory. We also address arguments against our characterization of autonoesis and argue that, while self-referential, it needs to be distinguished from an agentive notion of self. Regarding the function of episodic memory, we review arguments about the relation between future mental time travel and memory veridicality; clarify the relation between autonoesis, veridicality, and confidence; and finally discuss the role of episodic memory in diachronic commitments.
The hypoxic tumour microenvironment
Authors: Petrova Varvara , Annicchiarico-Petruzzelli Margherita , Melino Gerry , Amelio Ivano 
Published: January 2018

AbstractCancer progression often benefits from the selective conditions present in the tumour microenvironment, such as the presence of cancer-associated fibroblasts (CAFs), deregulated ECM deposition, expanded vascularisation and repression of the immune response. Generation of a hypoxic environment and activation of its main effector, hypoxia-inducible factor-1 (HIF-1), are common features of advanced cancers. In addition to the impact on tumour cell biology, the influence that hypoxia exerts on the surrounding cells represents a critical step in the tumorigenic process. Hypoxia indeed enables a number of events in the tumour microenvironment that lead to the expansion of aggressive clones from heterogeneous tumour cells and promote a lethal phenotype. In this article, we review the most relevant findings describing the influence of hypoxia and the contribution of HIF activation on the major components of the tumour microenvironment, and we summarise their role in cancer development and progression.
Unwrapping the genomic characteristics of urothelial bladder cancer and successes with immune checkpoint blockade therapy
Authors: Cheng Wen , Fu Dian , Xu Feng , Zhang Zhengyu 
Published: January 2018

AbstractUrothelial bladder cancer (UBC) is one of the most common lethal cancer worldwide and the 5-year survival rate has not improved significantly with current treatment protocols during the last decade. Intravesical immunotherapy with Bacillus Calmette-Guérin is currently the standard care for non-muscle invasive UBC. Recently, a subset of patients with locally advanced or metastatic UBC have responded to checkpoint blockade immunotherapy against the programmed cell death 1 protein (PD-1) or its ligand (PD-L1) or the cytotoxic T-lymphocyte antigen 4 that releases the inhibition of T cells, the remarkable clinical efficacy on UBC has brought total five checkpoint inhibitors approved by the FDA in the last 2 years, and this is revolutionizing treatment of advanced UBC. We discuss the rationale for immunotherapy in bladder cancer, progress with blocking the PD-1/PD-L1 pathway for UBC treatment, and ongoing clinical trials. We highlight the complexity of the interactions between cancer cells and the immune system, the genomic basis for response to checkpoint blockade immunotherapy, and potential biomarkers for predicting immunotherapeutic response.
Extracellular vesicle-mediated EBAG9 transfer from cancer cells to tumor microenvironment promotes immune escape and tumor progression
Authors: Miyazaki Toshiaki , Ikeda Kazuhiro , Sato Wataru , Horie-Inoue Kuniko , Inoue Satoshi 
Published: January 2018

AbstractThe antitumor immune response is a critical defense system that eliminates malignant cells. The failure of the system results in immune escape and proceeds to tumor growth. We have previously showed that estrogen receptor-binding fragment-associated antigen 9 (EBAG9) is a relevant cancer biomarker and facilities immune escape of cancers from the immune surveillance. EBAG9 in cancer cells suppresses T-cell infiltration into tumor in vivo, whereas that in host immune cells functions as a limiter for T-cell cytotoxicity. Considering that EBAG9 plays immune suppressive roles in both tumor and microenvironment, we here questioned whether EBAG9 is a transferable protein from cancer to surrounding T cells and affects antitumor immune response. In this study, we showed that spontaneous development of prostate cancer was repressed in a model of Ebag9 knockout mice crossed with transgenic adenocarcinoma of the mouse prostate (TRAMP) mice. We identified TM9SF1 as a collaborative EBAG9 interactor, which regulates epithelial-mesenchymal transition (EMT) in cancer cells. Notably, extracellular vesicles (EVs) from EBAG9-overexpressing prostate cancer cells have a potential to facilitate immune escape of tumors by inhibiting T-cell cytotoxicity and modulating immune-related gene expression in T cells. Furthermore, we showed that a neutralizing antibody for EBAG9 could rescue the EV-mediated immune suppression by recovering T-cell cytotoxicity. In addition to its autocrine functions in cancer cells, EBAG9 could behave as a new class of immune checkpoint that suppresses tumor immunity in a secretory manner. We propose that EBAG9-targeting cancer treatment could be alternative therapeutic options for advanced diseases, particularly for those with EBAG9 overexpression.
Subcortical evidence for a contribution of arousal to fMRI studies of brain activity
Authors: Liu Xiao , de Zwart Jacco A. , Schölvinck Marieke L. , Chang Catie , Ye Frank Q. , Leopold David A. , Duyn Jeff H. 
Published: January 2018

AbstractCortical activity during periods of rest is punctuated by widespread, synchronous events in both electrophysiological and hemodynamic signals, but their behavioral relevance remains unclear. Here we report that these events correspond to momentary drops in cortical arousal and are associated with activity changes in the basal forebrain and thalamus. Combining fMRI and electrophysiology in macaques, we first establish that fMRI transients co-occur with spectral shifts in local field potentials (LFPs) toward low frequencies. Applying this knowledge to fMRI data from the human connectome project, we find that the fMRI transients are strongest in sensory cortices. Surprisingly, the positive cortical transients occur together with negative transients in focal subcortical areas known to be involved with arousal regulation, most notably the basal forebrain. This subcortical involvement, combined with the prototypical pattern of LFP spectral shifts, suggests that commonly observed widespread variations in fMRI cortical activity are associated with momentary drops in arousal.
Discovery of new molecular entities able to strongly interfere with Hsp90 C-terminal domain
Authors: Terracciano Stefania , Russo Alessandra , Chini Maria G. , Vaccaro Maria C. , Potenza Marianna , Vassallo Antonio , Riccio Raffaele , Bifulco Giuseppe , Bruno Ines 
Published: January 2018

AbstractHeat shock protein 90 (Hsp90) is an ATP dependent molecular chaperone deeply involved in the complex network of cellular signaling governing some key functions, such as cell proliferation and survival, invasion and angiogenesis. Over the past years the N-terminal protein domain has been fully investigated as attractive strategy against cancer, but despite the many efforts lavished in the field, none of the N-terminal binders (termed “classical inhibitors”), currently in clinical trials, have yet successfully reached the market, because of the detrimental heat shock response (HSR) that showed to induce; thus, recently, the selective inhibition of Hsp90 C-terminal domain has powerfully emerged as a more promising alternative strategy for anti-cancer therapy, not eliciting this cell rescue cascade. However, the structural complexity of the target protein and, mostly, the lack of a co-crystal structure of C-terminal domain-ligand, essential to drive the identification of new hits, represent the largest hurdles in the development of new selective C-terminal inhibitors. Continuing our investigations on the identification of new anticancer drug candidates, by using an orthogonal screening approach, here we describe two new potent C-terminal inhibitors able to induce cancer cell death and a considerable down-regulation of Hsp90 client oncoproteins, without triggering the undesired heat shock response.
Restrained management of copper level enhances the antineoplastic activity of imatinib in vitro and in vivo
Authors: Hassan Iftekhar , Khan Azmat Ali , Aman Shazia , Qamar Wajhul , Ebaid Hossam , Al-Tamimi Jameel , Alhazza Ibrahim M. , Rady Ahmed M. 
Published: January 2018

AbstractThe present study was designed to investigate if elevated copper level can be targeted to enhance the efficacy of a significant anticancer drug, imatinib (ITB). The antineoplastic activity of this drug was assessed in the HepG2, HEK-293, MCF-7 and MDA-MD-231 cells targeting elevated copper level as their common drug target. The cell lines were treated with the different doses of copper chloride (Cu II) and disulfiram (DSF) alone as well as in their combinations with the drug for 24 h in standard culture medium and conditions. The treated cells were subjected to various assays including MTT, PARP, p-53, caspase-7, caspase-3, LDH and single cell electrophoresis. The study shows that DSF and Cu (II) synergizes the anticancer activity of ITB to a significant extent in a dose-specific way as evidenced by the combinations treated groups. Furthermore, the same treatment strategy was employed in cancer-induced rats in which the combinations of ITB-DSF and ITB-Cu II showed enhanced antineoplastic activity as compared to ITB alone. However, DSF was more effective than Cu (II) as an adjuvant to the drug. Hence, restrained manipulation of copper level in tumor cells can orchestrate the redox and molecular dispositions inside the cells favoring the induction of apoptosis.
Creating a mouse model resistant to induced ischemic stroke and cardiovascular damage
Authors: Ling Qing-Lan , Mohite Anita J. , Murdoch Emma , Akasaka Hironari , Li Qun-Ying , So Shui-Ping , Ruan Ke-He 
Published: January 2018

AbstractVascular prostanoids, isomerized from an intermediate prostaglandin (PG), H2, produced by cyclooxygenase (COX), exert various effects on the vascular system, both protective and destructive. During endothelial dysfunction, vascular protector prostacyclin/prostaglandin I2 (PGI2) is decreased, while inflammatory PGE2 and thrombotic TXA2 are increased. Therefore, our research aim was to reverse the event by controlling PGH2 metabolism by generating an in vivo model via enzymatic engineering of COX-1 and prostacyclin synthase (PGIS). The COX-1 and PGIS genes were linked to a 10-residue amino acid linker to form a Single-chain Enzyme Complex (SCHEC), COX-1-10aa-PGIS. Transgenic (CP-Tg) mice in a FVB/N background were generated using the pronuclear microinjection method. We first confirmed mRNA and protein expression of COX-1-10aa-PGIS in various CP-Tg mouse tissues, as well as upregulation of circulating PGI2. We then examined the cardiovascular function of these mice. Our CP-Tg mice exhibited marked resistance to vascular assault through induced carotid arterial blockage, acute thrombotic stroke and arterial arrest, angiotensin-induced peripheral vasoconstriction, and hepatic lipid accumulation after receiving a high-fat diet. They also had a longer lifespan compared with wild-type mice. This study raises the possibility of fighting cardiovascular diseases by regulating cellular arachidonic acid-derived PGH2 metabolites using enzymatic engineering.
Down-regulation of guanylate binding protein 1 causes mitochondrial dysfunction and cellular senescence in macrophages
Authors: Qiu Xiaoxue , Guo Hong , Yang Junshu , Ji Yinduo , Wu Chia-Shan , Chen Xiaoli 
Published: January 2018

AbstractMacrophage polarization is tightly associated with its metabolic reprograming and immune dysfunction. However, the intracellular molecules/pathways that connect these alterations in inflammatory macrophages remain largely unidentified. Herein, we explored the role of guanylate binding protein 1 (Gbp1), an intracellular anti-microbial protein, in regulating polarization, metabolic reprogramming, and cellular aging of macrophages. We showed that Gbp1 expression in inguinal white adipose tissue is significantly decreased in high-fat diet -fed and aged mice. Gbp1 expression is significantly induced by IFNγ and LPS in macrophages but not adipocytes. Downregulation of Gbp1 expression causes macrophage polarization towards a pro-inflammatory phenotype. Gbp1 knockdown (Kd) macrophages have impaired mitochondrial respiratory function, which is further supported by down-regulation of genes encoding electron transport chain components and genes involved in fatty acid oxidation and mitochondrial function. Moreover, we observed Gbp1 is localized in both cytosol and mitochondrial fraction, and Gbp1 Kd macrophages display decreased mitophagy activity. More interestingly, Gbp1 Kd macrophages undergo senescence as evidenced by increased activation of AMPK-p53 pathway and positive staining of β-galactosidase. These observations suggest that Gbp1 may play an important role in protecting against mitochondrial dysfunction and preserving immune function of macrophages during inflammatory stress and aging.
Predicting non-melanoma skin cancer via a multi-parameterized artificial neural network
Authors: Roffman David , Hart Gregory , Girardi Michael , Ko Christine J. , Deng Jun 
Published: January 2018

AbstractUltraviolet radiation (UVR) exposure and family history are major associated risk factors for the development of non-melanoma skin cancer (NMSC). The objective of this study was to develop and validate a multi-parameterized artificial neural network based on available personal health information for early detection of NMSC with high sensitivity and specificity, even in the absence of known UVR exposure and family history. The 1997–2015 NHIS adult survey data used to train and validate our neural network (NN) comprised of 2,056 NMSC and 460,574 non-cancer cases. We extracted 13 parameters for our NN: gender, age, BMI, diabetic status, smoking status, emphysema, asthma, race, Hispanic ethnicity, hypertension, heart diseases, vigorous exercise habits, and history of stroke. This study yielded an area under the ROC curve of 0.81 and 0.81 for training and validation, respectively. Our results (training sensitivity 88.5% and specificity 62.2%, validation sensitivity 86.2% and specificity 62.7%) were comparable to a previous study of basal and squamous cell carcinoma prediction that also included UVR exposure and family history information. These results indicate that our NN is robust enough to make predictions, suggesting that we have identified novel associations and potential predictive parameters of NMSC.