The partially alternating ternary sum in an associative dialgebra

The alternating ternary sum in an associative algebra, $abc - acb - bac + bca + cab - cba$, gives rise to the partially alternating ternary sum in an associative dialgebra with products $\dashv$ and $\vdash$ by making the argument $a$ the center of each term: $a \dashv b \dashv c - a \dashv c \dashv b - b \vdash a \dashv c + c \vdash a \dashv b + b \vdash c \vdash a - c \vdash b \vdash a$. We use computer algebra to determine the polynomial identities in degree $\le 9$ satisfied by this new trilinear operation. In degrees 3 and 5 we obtain $[a,b,c] + [a,c,b] \equiv 0$ and $[a,[b,c,d],e] + [a,[c,b,d],e] \equiv 0$; these identities define a new variety of partially alternating ternary algebras. We show that there is a 49-dimensional space of multilinear identities in degree 7, and we find equivalent nonlinear identities. We use the representation theory of the symmetric group to show that there are no new identities in degree 9.Comment: 14 page

Efficacy and safety of Elagolix in the treatment of endometriosis associated pain: a systematic review and network meta-analysis

Background: Endometriosis commonly presents with dysmenorrhea, non-menstrual pelvic pain, and infertility. Elagolix is an oral, short-acting, gonadotropin-releasing hormone antagonist acting through complete estrogen suppression. Objective: To evaluate the evidence from published randomized controlled trials (RCTs) about the efficacy and safety of Elagolix in the treatment of endometriosis associated pain. Search strategy: Electronic databases containing articles published between January 2000 and February 2020 were searched using the MeSH terms (Elagolix OR gonadotropin-releasing hormone antagonist OR GnRH antagonist OR antigonadotropin) AND (endometriosis) AND (pelvic pain). Selection criteria: All RCTs assessing the efficacy of Elagolix in the treatment of pain associated with endometriosis were considered for this network meta-analysis, where five studies were deemed eligible for this review. Data collection and analysis: The mean difference (MD) and confidence intervals (95% CI) for continuous outcomes including analgesic use, dysmenorrhea, non-menstrual pelvic pain, and quality of life were calculated. Main results: Elagolix 250 mg reduced dysmenorrhea significantly, as compared to placebo, (MD = -0.41, 95% CI [-0.7, -0.13]) at 12 weeks, while Elagolix 200 mg reduced dysmenorrhea significantly (MD= -1.2, 95% CI [-1.9, -0.57]) compared to placebo after 24 weeks of treatment. Conclusions: Elagolix 200 mg seems to be an effective drug with fewer side effects when used to reduce dysmenorrhea and non-menstrual pelvic pain after 24 weeks of treatment in patients with endometriosis

Synthesis of Gemini cationic surfactants based on natural nicotinic acid and evaluation of their inhibition performance at C-steel/1 M HCl interface: Electrochemical and computational investigations

Herein, we prepare effective Gemini cationic surfactants (CSII, CSIV) and characterize them using FT-IR and 1HNMR spectroscopy. The adsorptive properties of CSII and CSIV at HCl/air and C-steel/HCl interfaces were examined with surface tension and electrochemical parameters, respectively. The critical micelle concentration (CMC) of the CSII and CSIV indicated their adsorption affinity at the HCl/air interface. Where, aliphatic chains increase surface coverage percentage and aid in surfactant adsorption. The electrochemical parameters of C-steel in 1 M HCl were studied using electrochemical impedance spectroscopy (EIS) and potentiodynamic polarization (PDP) at different temperatures. The charge transfer resistance of the C-steel electrode was enhanced from 28.2 Ω.cm2 to 770.79 and 831.45 Ω.cm2 after adding 5 × 10−4 M of CSII and CSIV, respectively. Both CSII and CSIV act as mixed inhibitors with inhibition performance exceeding 97% due to their highly adsorption affinity. The chemical adsorption affinity of these compounds is suggested by the higher adsorption energy (∆G*ads) values (>−40 kJ mol−1) according to the Langmuir isotherm model. The theoretical calculations including DFT, and Monte Carlo simulation (MCs) provide insight into the relationship between corrosion inhibition and molecular structure, where the calculated parameters agree with the experimental results

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

Ion energy distribution functions behind the sheaths of magnetized and non magnetized radio frequency discharges

The effect of a magnetic field on the characteristics of capacitively coupled radio frequency discharges is investigated and found to be substantial. A one-dimensional particle-in-cell simulation shows that geometrically symmetric discharges can be asymmetrized by applying a spatially inhomogeneous magnetic field. This effect is similar to the recently discovered electrical asymmetry effect. Both effects act independently, they can work in the same direction or compensate each other. Also the ion energy distribution functions at the electrodes are strongly affected by the magnetic field, although only indirectly. The field influences not the dynamics of the sheath itself but rather its operating conditions, i.e., the ion flux through it and voltage drop across it. To support this interpretation, the particle-in-cell results are compared with the outcome of the recently proposed ensemble-in-spacetime algorithm. Although that scheme resolves only the sheath and neglects magnetization, it is able to reproduce the ion energy distribution functions with very good accuracy, regardless of whether the discharge is magnetized or not

Involvement of Autophagy in Cardiac Remodeling in Transgenic Mice with Cardiac Specific Over-Expression of Human Programmed Cell Death 5

Programmed cell death 5 (PDCD5) is a cytosolic protein suppressing growth of multiple types of cancer cells through activating p53. We hypothesized that PDCD5 plays an essential role in cardiac remodeling and function. PDCD5 was significantly up-regulated in the hearts from mice subjected to angiotensin II treatment or transverse aortic constriction. Thus, we generated transgenic mice over-expressing human PDCD5 under the control of alpha myosin heavy chain promoter to examine the role of PDCD5 in cardiac remodeling. Transgenic founder died spontaneously displayed enlarged heart. The high PDCD5 over-expressing line (10-fold) showed reduced survival rate, increase in heart weight normalized to body weight. Real-Time RT-PCR analysis revealed fetal gene program was up-regulated. Echocardiography and histopathological examination showed characteristics of dilated cardiomyopathy and heart failure in transgenic mice. Western blot and immunohistochemistry analysis showed autophagy was dramatically increased in transgenic mice as compared to WT littermates control mice, while apoptosis remained unchanged. The enhanced autophagy in high over-expressing line was associated with significant increase in p53 activity and its downstream target damage-regulated autophagy modulator expression. The low over-expressing line (3.5-fold) appeared normal, but was more susceptible to angiotensin II-induced cardiac hypertrophy. This study is the first providing evidence that PDCD5 plays an important role in cardiac remodeling

TBK1 Kinase Addiction in Lung Cancer Cells Is Mediated via Autophagy of Tax1bp1/Ndp52 and Non-Canonical NF-kappa B Signalling

K-Ras dependent non-small cell lung cancer (NSCLC) cells are 'addicted' to basal autophagy that reprograms cellular metabolism in a lysosomal-sensitive manner. Here we demonstrate that the xenophagy-associated kinase TBK1 drives basal autophagy, consistent with its known requirement in K-Ras-dependent NSCLC proliferation. Furthermore, basal autophagy in this context is characterised by sequestration of the xenophagy cargo receptor Ndp52 and its paralogue Tax1bp1, which we demonstrate here to be a bona fide cargo receptor. Autophagy of these cargo receptors promotes non-canonical NF-κB signalling. We propose that this TBK1-dependent mechanism for NF-κB signalling contributes to autophagy addiction in K-Ras driven NSCLC

Global burden of peripheral artery disease and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Background: Peripheral artery disease is a growing public health problem. We aimed to estimate the global disease burden of peripheral artery disease, its risk factors, and temporospatial trends to inform policy and public measures. Methods: Data on peripheral artery disease were modelled using the Global Burden of Disease, Injuries, and Risk Factors Study (GBD) 2019 database. Prevalence, disability-adjusted life years (DALYs), and mortality estimates of peripheral artery disease were extracted from GBD 2019. Total DALYs and age-standardised DALY rate of peripheral artery disease attributed to modifiable risk factors were also assessed. Findings: In 2019, the number of people aged 40 years and older with peripheral artery disease was 113 million (95% uncertainty interval [UI] 99·2–128·4), with a global prevalence of 1·52% (95% UI 1·33–1·72), of which 42·6% was in countries with low to middle Socio-demographic Index (SDI). The global prevalence of peripheral artery disease was higher in older people, (14·91% [12·41–17·87] in those aged 80–84 years), and was generally higher in females than in males. Globally, the total number of DALYs attributable to modifiable risk factors in 2019 accounted for 69·4% (64·2–74·3) of total peripheral artery disease DALYs. The prevalence of peripheral artery disease was highest in countries with high SDI and lowest in countries with low SDI, whereas DALY and mortality rates showed U-shaped curves, with the highest burden in the high and low SDI quintiles. Interpretation: The total number of people with peripheral artery disease has increased globally from 1990 to 2019. Despite the lower prevalence of peripheral artery disease in males and low-income countries, these groups showed similar DALY rates to females and higher-income countries, highlighting disproportionate burden in these groups. Modifiable risk factors were responsible for around 70% of the global peripheral artery disease burden. Public measures could mitigate the burden of peripheral artery disease by modifying risk factors. Funding: Bill & Melinda Gates Foundation