All Multiparty Quantum States Can Be Made Monogamous

Monogamy of quantum correlation measures puts restrictions on the sharability of quantum correlations in multiparty quantum states. Multiparty quantum states can satisfy or violate monogamy relations with respect to given quantum correlations. We show that all multiparty quantum states can be made monogamous with respect to all measures. More precisely, given any quantum correlation measure that is non-monogamic for a multiparty quantum state, it is always possible to find a monotonically increasing function of the measure that is monogamous for the same state. The statement holds for all quantum states, whether pure or mixed, in all finite dimensions and for an arbitrary number of parties. The monotonically increasing function of the quantum correlation measure satisfies all the properties that is expected for quantum correlations to follow. We illustrate the concepts by considering a thermodynamic measure of quantum correlation, called the quantum work deficit.Comment: 6.5 pages, 2 figures, RevTeX 4-1, Title in the published version is "Monotonically increasing functions of any quantum correlation can make all multiparty states monogamous

Prevalence of refractive errors in children in India: a systematic review

Uncorrected refractive error is an avoidable cause of visual impairment which affects children in India. The objective of this review is to estimate the prevalence of refractive errors in children ≤ 15 years of age. The Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines were followed in this review. A detailed literature search was performed to include all population and school‐based studies published from India between January 1990 and January 2017, using the Cochrane Library, Medline and Embase. The quality of the included studies was assessed based on a critical appraisal tool developed for systematic reviews of prevalence studies. Four population‐based studies and eight school‐based studies were included. The overall prevalence of refractive error per 100 children was 8.0 (CI: 7.4–8.1) and in schools it was 10.8 (CI: 10.5–11.2). The population‐based prevalence of myopia, hyperopia (≥ +2.00 D) and astigmatism was 5.3 per cent, 4.0 per cent and 5.4 per cent, respectively. Combined refractive error and myopia alone were higher in urban areas compared to rural areas (odds ratio [OR]: 2.27 [CI: 2.09–2.45]) and (OR: 2.12 [CI: 1.79–2.50]), respectively. The prevalence of combined refractive errors and myopia alone in schools was higher among girls than boys (OR: 1.2 [CI: 1.1–1.3] and OR: 1.1 [CI: 1.1–1.2]), respectively. However, hyperopia was more prevalent among boys than girls in schools (OR: 2.1 [CI: 1.8–2.4]). Refractive error in children in India is a major public health problem and requires concerted efforts from various stakeholders including the health care workforce, education professionals and parents, to manage this issue

Medicina clínica práctica

Today one cannot think of life without the Internet. The Internet has grown at a very fast pace, which has resulted in heavy Internet traffic. Most of today’s internet traffic is due to video streaming services such as YouTube and Netflix. The Average traffic load has risen, and data traffic patterns have also become unpredictable. Therefore, network traffic monitoring and analysis have become essential in order to troubleshoot and resolve problems effectively when they occur, so that network services do not stand still for long durations of time. Traffic monitoring is a technique which constantly monitors the network traffic and notifies the administrator whenever there is an outage. There are many network monitoring tools available for network administrators, which use different monitoring techniques in order to monitor and analyze network traffic. In this paper, we present different network monitoring approaches and different tools that monitor and analyze network traffic. In addition to this, we also present results by comparing different network monitoring tools

Exploration of multifaceted molecular mechanism of angiotensin-converting enzyme 2 (ACE2) in pathogenesis of various diseases

Angiotensin converting enzyme 2 (ACE2) is a homolog of ACE (a transmembrane bound dipeptidyl peptidase enzyme). ACE2 converts angiotensinogen to the heptapeptide angiotensin-(1–7). ACE2 and its product, angiotensin-(1–7), have counteracting effects against the adverse actions of other members of renin-angiotensin system (RAS). ACE2 and its principal product, angiotensin-(1–7), were considered an under recognized arm of the RAS. The COVID-19 pandemic brought to light this arm of RAS with special focus on ACE2. Membrane bound ACE2 serves as a receptor for SARS-CoV-2 viral entry through spike proteins. Apart from that, ACE2 is also involved in the pathogenesis of various other diseases like cardiovascular disease, cancer, respiratory diseases, neurodegenerative diseases and infertility. The present review focuses on the molecular mechanism of ACE2 in neurodegenerative diseases, cancer, cardiovascular disease, infertility and respiratory diseases, including SARS-CoV-2. This review summarizes unveiled roles of ACE2 in the pathogenesis of various diseases which further provides intriguing possibilities for the use of ACE2 activators and RAS modulating agents for various diseases

Analysmetoder för fastställande av 60 spårelement i klosettvatten

Klosettvatten är en bra växtnäringskälla vid odling av energi- och fodergrödor, med kvalitet motsvarande nötflytgödsel ur växtnärings- och tungmetallsynpunkt. Genom att välja en kraftigare uppslutningsmetod, vätefluorid och salpetersyra, i kombination med matrisseparering, kan cirka 48 spårelement kvantifieras istället för ett tjugotal med dagens konventionella metoder

A complete map of the Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) signaling pathway

Calcium/calmodulin-dependent protein kinase kinase 2 (CAMKK2) is a serine/threonine-protein kinase belonging to the Ca2+/calmodulin-dependent protein kinase subfamily. CAMKK2 has an autocatalytic site, which gets exposed when Ca2+/calmodulin (CAM) binds to it. This results in autophosphorylation and complete activation of CAMKK2. The three major known downstream targets of CAMKK2 are 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPKα), calcium/calmodulin-dependent protein kinase 1 (CAMK1) and calcium/calmodulin-dependent protein kinase 4 (CAMK4). Activation of these targets by CAMKK2 is important for the maintenance of different cellular and physiological processes within the cell. CAMKK2 is found to be important in neuronal development, bone remodeling, adipogenesis, and systemic glucose homeostasis, osteoclastgensis and postnatal myogensis. CAMKK2 is reported to be involved in pathologies like Duchenne muscular dystrophy, inflammation, osteoporosis and bone remodeling and is also reported to be overexpressed in prostate cancer, hepatic cancer, ovarian and gastric cancer. CAMKK2 is involved in increased cell proliferation and migration through CAMKK2/AMPK pathway in prostate cancer and activation of AKT in ovarian cancer. Although CAMKK2 is a molecule of great importance, a public resource of the CAMKK2 signaling pathway is currently lacking. Therefore, we carried out detailed data mining and documentation of the signaling events associated with CAMKK2 from published literature and developed an integrated reaction map of CAMKK2 signaling. This resulted in the cataloging of 285 reactions belonging to the CAMKK2 signaling pathway, which includes 33 protein-protein interactions, 74 post-translational modifications, 7 protein translocation events, and 22 activation/inhibition events. Besides, 124 gene regulation events and 25 activator/inhibitors involved in CAMKK2 activation were also cataloged. The CAMKK2 signaling pathway map data is made freely accessible through WikiPathway database ( https://www.wikipathways.org/index.php/Pathway:WP4874 ). We expect that data on a signaling map of CAMKK2 will provide the scientific community with an improved platform to facilitate further molecular as well as biomedical investigations on CAMKK2 and its utility in the development of biomarkers and therapeutic targets

Stapled Peptides as Direct Inhibitors of Nrf2-sMAF Transcription Factors

Nuclear factor erythroid-related 2-factor 2 (Nrf2) is a transcription factor traditionally thought of as a cellular protector. However, in many cancers, Nrf2 is constitutively activated and correlated with therapeutic resistance. Nrf2 heterodimerizes with small musculoaponeurotic fibrosarcoma Maf (sMAF) transcription factors, allowing binding to the antioxidant responsive element (ARE) and induction of transcription of Nrf2 target genes. While transcription factors are historically challenging to target, stapled peptides have shown great promise for inhibiting these protein–protein interactions. Herein, we describe the first direct cell-permeable inhibitor of Nrf2/sMAF heterodimerization. N1S is a stapled peptide designed based on AlphaFold predictions of the interactions between Nrf2 and sMAF MafG. A cell-based reporter assay combined with in vitro biophysical assays demonstrates that N1S directly inhibits Nrf2/MafG heterodimerization. N1S treatment decreases the transcription of Nrf2-dependent genes and sensitizes Nrf2-dependent cancer cells to cisplatin. Overall, N1S is a promising lead for the sensitization of Nrf2-addicted cancers

Stapled Peptides as Direct Inhibitors of Nrf2-sMAF Transcription Factors

Nuclear factor erythroid-related 2-factor 2 (Nrf2) is a transcription factor traditionally thought of as a cellular protector. However, in many cancers, Nrf2 is constitutively activated and correlated with therapeutic resistance. Nrf2 heterodimerizes with small musculoaponeurotic fibrosarcoma Maf (sMAF) transcription factors, allowing binding to the antioxidant responsive element (ARE) and induction of transcription of Nrf2 target genes. While transcription factors are historically challenging to target, stapled peptides have shown great promise for inhibiting these protein–protein interactions. Herein, we describe the first direct cell-permeable inhibitor of Nrf2/sMAF heterodimerization. N1S is a stapled peptide designed based on AlphaFold predictions of the interactions between Nrf2 and sMAF MafG. A cell-based reporter assay combined with in vitro biophysical assays demonstrates that N1S directly inhibits Nrf2/MafG heterodimerization. N1S treatment decreases the transcription of Nrf2-dependent genes and sensitizes Nrf2-dependent cancer cells to cisplatin. Overall, N1S is a promising lead for the sensitization of Nrf2-addicted cancers