Miracle-dz/UniFAR-FTUs huggingface dataset:
Energy Deficit Required for Rapid Weight Loss in Elite Collegiate Wrestlers

To determine energy density for rapid weight loss (RWL) of weight-classified sports, eight male elite wrestlers were instructed to lose 6% of body mass (BM) within 53 h. Energy deficit during the RWL was calculated by subtracting total energy expenditure (TEE) determined using the doubly labeled water method (DLW) from energy intake (EI) assessed with diet records. It was also estimated from body composition change estimated with the four-component model (4C) and other conventional methods. BM decreased significantly by 4.7 ± 0.5 kg (6.4 ± 0.5%). Total body water loss was the major component of the BM loss (71.0 ± 7.6%). TEE was 9446 ± 1422 kcal, and EI was 2366 ± 1184 kcal during the RWL of 53-h; therefore, the energy deficit was 7080 ± 1525 kcal. Thus, energy density was 1507 ± 279 kcal/kg ∆BM during the RWL, comparable with values obtained using the 4C, three-component model, dual energy X-ray absorptiometry, and stable isotope dilution. Energy density for RWL of wrestlers is lower than that commonly used (7400 or 7700 kcal/kg ΔBM). Although RWL is not recommended, we propose that commonly practiced extreme energy restriction such as 7400 or 7700 kcal/kg ΔBM during RWL appears to be meaningless.
R-Ras1 and R-Ras2 Are Essential for Oligodendrocyte Differentiation and Survival for Correct Myelination in the Central Nervous System

Rapid and effective neural transmission of information requires correct axonal myelination. Modifications in myelination alter axonal capacity to transmit electric impulses and enable pathological conditions. In the CNS, oligodendrocytes (OLs) myelinate axons, a complex process involving various cellular interactions. However, we know little about the mechanisms that orchestrate correct myelination. Here, we demonstrate that OLs express R-Ras1 and R-Ras2. Using female and male mutant mice to delete these proteins, we found that activation of the PI3K/Akt and Erk1/2-MAPK pathways was weaker in mice lacking one or both of these GTPases, suggesting that both proteins coordinate the activity of these two pathways. Loss of R-Ras1 and/or R-Ras2 diminishes the number of OLs in major myelinated CNS tracts and increases the proportion of immature OLs. In R-Ras1−/− and R-Ras2−/−-null mice, OLs show aberrant morphologies and fail to differentiate correctly into myelin-forming phenotypes. The smaller OL population and abnormal OL maturation induce severe hypomyelination, with shorter nodes of Ranvier in R-Ras1−/− and/or R-Ras2−/− mice. These defects explain the slower conduction velocity of myelinated axons that we observed in the absence of R-Ras1 and R-Ras2. Together, these results suggest that R-Ras1 and R-Ras2 are upstream elements that regulate the survival and differentiation of progenitors into OLs through the PI3K/Akt and Erk1/2-MAPK pathways for proper myelination. SIGNIFICANCE STATEMENT In this study, we show that R-Ras1 and R-Ras2 play essential roles in regulating myelination in vivo and control fundamental aspects of oligodendrocyte (OL) survival and differentiation through synergistic activation of PI3K/Akt and Erk1/2-MAPK signaling. Mice lacking R-Ras1 and/or R-Ras2 show a diminished OL population with a higher proportion of immature OLs, explaining the observed hypomyelination in main CNS tracts. In vivo electrophysiology recordings demonstrate a slower conduction velocity of nerve impulses in the absence of R-Ras1 and R-Ras2. Therefore, R-Ras1 and R-Ras2 are essential for proper axonal myelination and accurate neural transmission.
Dopamine dysfunction in 22q11 deletion syndrome: possible cause of motor symptoms

22q11 Deletion syndrome (22q11DS) is a neurogenetic disorder, resulting from a hemizygous microdeletion on the long arm of chromosome 22. In 22q11DS, the phenotypic expression is highly variable. Approximately one-third of all individuals with 22q11DS develop schizophrenia-like psychotic disorder. Among the genes in the deleted region, catechol-O-methyltransferase (COMT) has a particular relevance for psychiatric disorders: lower COMT enzymatic activity decreases the clearance of dopamine (DA), yielding higher levels of catecholamines in the central nervous system. Deficits in myelinogenesis and dysfunctions in the DA system could justify the white matter abnormalities in motor/premotor circuits described in 22q11DS. The alterations in DA could determine the high incidence of psychiatric disorders and the presence of neurological soft signs in 22q11DS. Neurological soft signs are defined as non-normative performance on an examination of motor and sensory tasks without focal neurological deficits. COMT haploinsufficiency, DA dysfunction, and white matter abnormalities may contribute toward the presence of neurological soft signs in 22q11DS.
WNT signalling events near the cell membrane and their pharmacological targeting for the treatment of cancer

WNT signalling is an essential signalling pathway for all multicellular animals. Although first described more than 30 years ago, new components and regulators of the pathway are still being discovered. Considering its importance in both embryonic development and adult homeostasis, it is not surprising that this pathway is often deregulated in human diseases such as cancer. Recently, it became clear that in addition to cytoplasmic components such as β‐catenin, other, membrane‐bound or extracellular, components of the WNT pathway are also altered in cancer. This review gives an overview of the recent discoveries on WNT signalling events near the cell membrane. Furthermore, membrane‐associated components of the WNT pathway, which are more accessible for therapeutic intervention, as well therapeutic approaches that already target those components will be discussed. In this way, we hope to stimulate the development of effective anti‐cancer therapies that target this fascinating pathway.
Determination of the electric vehicles driving modes in real life conditions by classification methods

In order to study the aging of batteries in automotive applications, it is important to understand how and under what conditions these batteries are operating in electric vehicles (EVs). However, because of the specificities of EVs, these uses may be very different from those known from internal combustion engine cars (ICE). In this paper, we present how, from real-life data, we determine the different driving modes of electric vehicles. The paper presents the different techniques adopted to analyze and classify the data and the different EV running modes, which are obtained.
Lifelong reduction in complex IV induces tissue‐specific metabolic effects but does not reduce lifespan or healthspan in mice

Loss of SURF1, a Complex IV assembly protein, was reported to increase lifespan in mice despite dramatically lower cytochrome oxidase (COX) activity. Consistent with this, our previous studies found advantageous changes in metabolism (reduced adiposity, increased insulin sensitivity, and mitochondrial biogenesis) in Surf1−/− mice. The lack of deleterious phenotypes in Surf1−/− mice is contrary to the hypothesis that mitochondrial dysfunction contributes to aging. We found only a modest (nonsignificant) extension of lifespan (7% median, 16% maximum) and no change in healthspan indices in Surf1−/− vs. Surf1+/+ mice despite substantial decreases in COX activity (22%–87% across tissues). Dietary restriction (DR) increased median lifespan in both Surf1+/+ and Surf1−/− mice (36% and 19%, respectively). We measured gene expression, metabolites, and targeted expression of key metabolic proteins in adipose tissue, liver, and brain in Surf1+/+ and Surf1−/− mice. Gene expression was differentially regulated in a tissue‐specific manner. Many proteins and metabolites are downregulated in Surf1−/− adipose tissue and reversed by DR, while in brain, most metabolites that changed were elevated in Surf1−/− mice. Finally, mitochondrial unfolded protein response (UPRmt)‐associated proteins were not uniformly altered by age or genotype, suggesting the UPRmt is not a key player in aging or in response to reduced COX activity. While the changes in gene expression and metabolism may represent compensatory responses to mitochondrial stress, the important outcome of this study is that lifespan and healthspan are not compromised in Surf1−/− mice, suggesting that not all mitochondrial deficiencies are a critical determinant of lifespan.
Characterization of highly pathogenic avian influenza H5N8 virus from Egyptian domestic waterfowl in 2017

ABSTRACT In 2016, the highly pathogenic avian influenza (HPAI) H5N8 virus was detected in wild birds for the first time in Egypt. In the present study, we identified the HPAI virus H5N8 of clade 2.3. 4.4 from domestic waterfowl in Egypt, suggesting its transmission to the domestic poultry from the migratory birds. Based on partial haemagglutinin gene sequence, this virus has a close genetic relationship with subtype H5N8 viruses circulating in Asia and Europe. Pathologically, H5N8 virus in hybrid duck induced nervous signs accompanied by encephalomalacia, haemorrhages, nonsuppurative encephalitis and nonsuppurative vasculitis. The granular layer of cerebellum showed multifocal areas of hydropic degeneration and the Purkinje cell neurons were necrotized or lost. Additionally, the lung, kidney and spleen were congested, and necrotizing pancreatitis was also observed. The co-circulation of both HPAI H5N1 and H5N8 subtypes with the low pathogenic avian influenza H9N2 subtype complicate the control of avian influenza in Egypt with the possibility of emergence of new reassortant viruses. Therefore, continuous monitoring with implementation of strict control measures is required. Research highlights HPAI H5N8 virus clade 2.3. 4.4 was detected in domestic ducks and geese in Egypt in 2017. Phylogenetically, the virus was closely related to HPAI H5N8 viruses identified in Asia and Europe Nonsuppurative encephalitis was widely observed in HPAI H5N8 virus-infected ducks. Degeneration of the cerebellar granular layer was found in most of the brain tissues examined.
Longitudinal Effects of Increases and Decreases in Intimate Partner Aggression

Interventions aimed at reducing interpartner aggression assume that within-couple declines in aggression enhance individual and relational outcomes, yet reductions in aggression may fail to yield these benefits when other risk-generating mechanisms remain intact. The present study evaluates this possibility by investigating whether naturally observed within-couple changes in aggression are associated with improved individual and relational outcomes in the manner assumed by intervention programs. Drawing upon 4 waves of data collected at 9-month intervals from a community sample of 431 newlywed couples (76% Hispanic) living in low-income neighborhoods, Actor-Partner-Interdependence Modeling (APIM) and Structural Equation Modeling (SEM) indicated that levels of aggression at the outset of marriage had limited associations with later outcomes. Changes in aggression, however, were associated with subsequent marital outcomes, such that decreases in aggression were beneficial and increases in aggression were costly. Individuals who experienced increases in aggression worsened in their observed communication over time and reported greater increases in stress. Reports of stress early in marriage predicted escalations in aggression over time. Thus, helping couples to contain increases in aggression might be particularly consequential for their well-being.
Size, Value and Momentum in Pakistan Equity Markets: Size and Liquidity Exposures

The study inspects the size and liquidity pattern in Pakistan equity market. Sample size contains 278 non-financial firm's monthly data listed on Pakistan Stock Exchange (PSX) from 2001 to 2012. This study uses three asset pricing models (eq.5), (eq.6) and (eq.7). Four factors asset pricing model estimates that momentum factor is positively and negatively linked with winner and loser stocks, both in size and liquidity patterns. Although it is observed that the presence of size and liquidity does not affect the coefficient results but average value of momentum premium in larger in liquidity than size pattern. Further, the study reveals high average stock returns on momentum strategy in liquidity pattern than size that is 8.05% Vs 6.67%, respectively. Results of this study contradicts Fama and French (2012) who concluded that size pattern in momentum factor outperform the equity market. But this study conclude that liquidity pattern outperforms the size pattern in momentum factor. This study raises the question that should investors and academicians consider size or liquidity pattern in momentum factor for high returns and future research?
Treatment schedule is of importance when gefitinib is combined with irradiation of glioma and endothelial cells in vitro

Amplified epidermal growth factor receptor (EGFR) signaling is supposed to contribute to clinical radiation resistance of glioblastoma multiforme (GBM). Therefore, inhibition of EGFR signaling pathways by the selective EGFR tyrosine kinase inhibitor, gefitinib (ZD1839, Iressa), may increase the therapeutic effects of radiotherapy. The effects of different schedules for administration of gefitinib on sensitivity to irradiation of the human glioma cell lines (251MG and SF-767), a rat glioma cell line (BT4C), and an immortalized rat brain endothelial cell line (RBE4) is reported. Differences in effects of the combined treatment on cell toxicity were determined by a fluorometric cytotoxicity assay, and nuclear DNA fragmentation was used for quantification of apoptosis. Pre-administration with gefitinib for 30 min prior to irradiation followed by continuous incubation with gefitinib significantly increased the cytotoxicity of SF-767, BT4C, and RBE4 cells. However, the human glioma cell line 251MG was protected against radiation-induced damage by this treatment schedule, at lower concentrations of gefitinib. Pre-administration with gefitinib for 24 h prior to irradiation without following incubation with gefitinib increased the cytotoxicity of SF-767 and BT4C cells. Post-irradiation treatment with gefitinib significantly increased the cytotoxicity in all cell lines except for 251MG. We demonstrated heterogeneity in the cytotoxic effects of gefitinib between cell lines. Response to gefitinib might be due to other mechanisms than through the EGF receptor as some of the cell lines showed sensitivity to gefitinib despite no or low expression of EGFR. This study also demonstrates the importance of timing of gefitinib administration when this agent is combined with irradiation.
Singled Out as the Effect to be Explained

The description and explanation of intergroup differences tend to be framed in terms of how nonnormative (untypical and/or stigmatized) groups differ from normative groups rather than vice versa. Three experiments examined how this affects group members’ collective self-esteem. Single participants felt worse about being single when they read (Study 1) or wrote (Study 2) about how singles differ from coupled people than when they read or wrote about how coupled people differ from singles—although they mentioned more positive aspects of being single under the former comparative framing. In Study 3, left-handed participants indicated lower private collective self-esteem after writing about how left-handers differ from right-handers than after writing about how right-handers differ from left-handers. Thus, regardless of the specific characteristics that the comparison focused on, being marked as different and having to explain one’s group identity negatively affected members of nonnormative, but not members of normative groups.
DNA Damage Induced by 4,6,8,9-Tetramethyl-2H-furo[2,3-h]quinolin-2-one, a New Furocoumarin Analog: Biological Consequences

Abstract 4,6,8,9-Tetramethyl-2H-furo[2,3-h]quinolin-2-one (HFQ) and its isomer FQ (1,4,6,8-tetramethyl-2H-furo[2,3-h]quinolin-2-one) showed very strong antiproliferative activity in mammalian cells, about two times greater than 8-methoxypsoralen (8-MOP). Both compounds induced DNA–protein cross-links (DPC) but not interstrand cross-links. The FQ generated DPC in a biphotonic process, yielding a new kind of diadduct, whereas HFQ induced DPC by a monophotonic one, probably without its physical participation in the covalent bridge. These lesions gave different toxic responses. Sensitization of FQ led to extensive DNA fragmentation and to a number of chromosomal aberrations. Conversely, HFQ seemed to be completely inactive and 8-MOP gave intermediate results. A strict relationship between DPC formation and induction of chromosomal aberrations was observed. The HFQ did not induce light skin erythemas, whereas FQ was more phototoxic than 8-MOP, thus suggesting that FQ lesions, DPC in particular, may be implicated in skin phototoxicity. Ehrlich ascites cells, a transplantable mouse tumor, inactivated by furoquinolinone sensitization and injected into healthy mice, protected them from a successive challenge by viable tumor cells. This response appeared to be based on an immune mechanism. Comparable amounts of base substitution revertants were scored when testing furoquinolinones and 8-MOP in bacteria but no DPC were detected. This suggests that classic mutagenesis tests on bacteria are insufficient to give adequate information on furocoumarin genotoxicity. Given its features, HFQ can be regarded as an interesting new agent for psoralen plus UVA photochemotherapy and photopheresis.
“Fear promotes the status quo” : surveillance discourses and environmental activism in Canada

This paper explores the topics of state surveillance and democratic participation. It examines how targeted surveillance—backed by the implicit threat of state violence—shapes the behaviour and sense of identity of Canadian activists who express dissent to dominant economic, technological, or cultural modes. In particular, the project focuses on members of the environmental movement who have, in legally permissible ways, expressed opposition to critical infrastructure (CI) projects such as pipelines or dams. In Canada, among other nations, the inclusion of CI protection in national security priorities has enabled the surveillance of such environmental activists, treating them as a potential threat. Knowledge of state-sanctioned surveillance has become widespread, reinforcing the need for even law-abiding CI opponents to locate themselves within the discourse of this exercise and reinforcement of state power and the categories it implies. My research, then, seeks to determine what influence, if any, targeted state surveillance has on the identity performance of law-abiding environmental activists in Canada. Through a critical discourse analysis of such activists’ interview responses, the project investigates how the surveillance context has influenced the way activists understand and discuss lawful expressions of dissent and their own role in society.
Fine‐needle aspiration cytology of mammary fibroadenoma: A comparison of ThinPrep® and cytospin preparations

Mammary fibroadenoma (FA) is a lesion frequently sampled and diagnosed by fine‐needle aspiration (FNA). Accurate cytologic diagnosis of this common benign lesion is important as this can lead to non‐surgical, conservative management when breast imaging and clinical examination are concordant. In most instances, a confident diagnosis of FA is possible because of a characteristic cytologic appearance that includes hypercellularity, large epithelial cell groups, staghorn epithelial configurations, stromal fragments, and numerous background stripped nuclei. 1 , 2 Nevertheless, FAs can be diagnostically challenging because of shared cytomorphologic features with other benign lesions and low‐grade carcinoma. As such, FA is a well‐recognized source of false results on FNA cytology. 2–10 Furthermore, there are reports that newer thin layer cytopreparatory techniques, including the ThinPrep® (TP) system (Hologic Corp., Bedford, MA), alter the appearance of FA on FNA compared to conventional preparations and may compromise accurate cytologic diagnosis. 11–13 Diagn. Cytopathol. 2011;39:181–187. © 2010 Wiley‐Liss, Inc.
Serum levels of neopterin, tumor necrosis factor-alpha and Interleukin-6 in preeclampsia: relationship with disease severity.

AIM There are many studies evaluating the role of inflammation in the pathogenesis of preeclampsia. However, little is known about the relationship between the severity of inflammation and the severity of preeclampsia due to insufficient of studies reporting this matter. To investigate the maternal serum concentrations of IL-6, TNF-alpha and Neopterin in patients with mild preeclampsia and severe preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome in preeclampsia and determine their association with the severity of the disease. PATIENTS AND METHODS Patients, hospitalized with the diagnosis of preeclampsia between October 2011 and March 2012, were included in the study. The patients with preeclampsia were divided into three groups as mild preeclampsia, severe preeclampsia and HELLP syndrome. The control group was comprised of normotensive and uncomplicated pregnant women. The serum levels of IL-6, TNF-alpha and Neopterin (NEO) were determined, using enzyme-linked immunosorbent assay. Spearman's rank correlation tests were used for the correlations between the serum levels of inflammatory markers and the severity of preeclampsia. RESULTS There was no observed significant difference among mean serum TNF-alpha and IL-6 levels of four groups (p > 0.05). The median serum concentration of NEO in subjects with mild preeclampsia of 14.1 nmol/L and severe preeclampsia of 14.8 nmol/L was significantly higher than that of 10.3 nmol/L in normotensive controls (p = 0.013; p = 0.000 respectively). In addition, the median serum concentration of NEO was detected to be highest in subjects with HELLP syndrome. The serum levels of NEO was well correlated with the severity of preeclampsia (r = 0.533, p = 0.000). CONCLUSIONS The serum levels of NEO, an important marker of cellular immunity, associated with severity of disease in patients with preeclampsia.
PMN-MDSC and arginase are increased in myeloma and may contribute to resistance to therapy

ABSTRACT Objectives: Despite improvement in overall response due to the introduction of the first-in-class proteasome inhibitor bortezomib (btz), multiple myeloma (MM) is still an incurable disease due to the immune-suppressive bone marrow (BM) environment. Thus, the authors aimed to identify the role of CD11b+CD15+CD14−HLA-DR− granulocytic-like myeloid-derived suppressor cells (PMN-MDSC) in MM patients treated up-front with novel agents. Methods: In MM cell lines and primary cells derived by patients affected by MGUS and MM, we investigated sensitivity to bortezomib and lenalidomide in presence of Arg-1 and PMN-MDSC. Results: The authors found that PMN-MDSC and their function through increased arginase-1 (Arg-1) are associated with MM progression. When the authors assessed cell viability of the human myeloma cell lines MM1.s, OPM2 and U266 treated with 5–20 nM btz for 24 h in PMN-MDSC conditioned media, they disclosed that amount of Arg-1 and Arg-1 inhibition could affect btz sensitivity in-vitro. PMN-MDSC and Arg-1 were increased in peripheral blood of newly diagnosed MM patients compared to healthy subjects. PMN-MDSC and arginase were reduced after exposure to lenalidomide-based regimen but increased after btz-based treatment. Conclusion: In MM, Arg-1 is mainly expressed by PMN-MDSC. PMN-MDSC and Arg-1 are reduced in vivo after lenalidomide but not bortezomib treatment.