The Causal Nexus Between Different Feed Networks and Defected Ground Structures in Multi-Port MIMO Antennas.

Multiple input multiple output (MIMO) antennas have recently received attention for improving wireless communication data rates in rich scattering environments. Despite this, the challenge of isolation persists prominently in compact MIMO-based electronics. Various techniques have recently emerged to address the isolation issues, among which the defected ground structure (DGS) stands out as a cost-effective solution.

Inflammatory crosstalk impairs phagocytic receptors and aggravates atherosclerosis in clonal hematopoiesis in mice.

Clonal hematopoiesis (CH) increases inflammasome-linked atherosclerosis, but the mechanisms by which CH mutant cells transmit inflammatory signals to nonmutant cells are largely unknown. To address this question, we transplanted 1.5% Jak2V617F (Jak2VF) bone marrow (BM) cells with 98.

The Impact of Deep Learning on Determining the Necessity of Bronchoscopy in Pediatric Foreign Body Aspiration: Can Negative Bronchoscopy Rates Be Reduced?

Introduction: This study aimed to evaluate the role of deep learning methods in diagnosing foreign body aspiration (FBA) to reduce the frequency of negative bronchoscopy and minimize potential complications.

Methods: We retrospectively analysed data and radiographs from 47 pediatric patients who presented to our hospital with suspected FBA between 2019 and 2023. A control group of 63 healthy children provided a total of 110 PA CXR images, which were analysed using both convolutional neural network (CNN)-based deep learning methods and multiple logistic regression (MLR).

Genetic and epigenetic regulation of inflammasomes: Role in atherosclerosis.

The cardiovascular complications of atherosclerosis are thought to arise from an inflammatory response to the accumulation of cholesterol-rich lipoproteins in the arterial wall. The positive outcome of CANTOS (Canakinumab Anti-inflammatory Thrombosis Outcome Study) provided key evidence to support this concept and suggested that inflammasomes and IL-1β are important inflammatory mediators in human atherosclerotic cardiovascular diseases (ACVD). In specific settings NLRP3 or AIM2 inflammasomes can induce inflammatory responses in the arterial wall and promote the formation of unstable atherosclerotic plaques.

Cholesterol trafficking to the ER leads to the activation of CaMKII/JNK/NLRP3 and promotes atherosclerosis.

The deposition of cholesterol-rich lipoproteins in the arterial wall triggers macrophage inflammatory responses, which promote atherosclerosis. The NLRP3 inflammasome aggravates atherosclerosis; however, cellular mechanisms connecting macrophage cholesterol accumulation to inflammasome activation are poorly understood. We investigated the mechanisms of NLRP3 inflammasome activation in cholesterol-loaded macrophages and in atherosclerosis-prone Ldlr mice with defects in macrophage cholesterol efflux.

Jak2 V617F clonal hematopoiesis promotes arterial thrombosis via platelet activation and cross talk.

JAK2 V617F (JAK2VF) clonal hematopoiesis (CH) has been associated with atherothrombotic cardiovascular disease (CVD). We assessed the impact of Jak2VF CH on arterial thrombosis and explored the underlying mechanisms. A meta-analysis of 3 large cohort studies confirmed the association of JAK2VF with CVD and with platelet counts and adjusted mean platelet volume (MPV).

Sphingosine-1-phosphate receptor 3 regulates the transendothelial transport of high-density lipoproteins and low-density lipoproteins in opposite ways.

Aims: The entry of lipoproteins from blood into the arterial wall is a rate-limiting step in atherosclerosis. It is controversial whether this happens by filtration or regulated transendothelial transport.Because sphingosine-1-phosphate (S1P) preserves the endothelial barrier, we investigated in vivo and in vitro, whether S1P and its cognate S1P-receptor 3 (S1P3) regulate the transendothelial transport of lipoproteins.

The Evaluation of Different Treatment Approaches in Patients With Earthquake-Related Crush Syndrome.

Background: On February 6, 2023, an earthquake occurred in Kahramanmaras, Turkey, resulting in loss of life, injuries, and the displacement of thousands of people. The aim of this study is to determine the factors affecting amputation and fasciotomy decisions in patients with crush syndrome, along with clinical laboratory parameters.

Materials And Methods: The study included patients over 18 years of age who presented with crush injuries and exhibited systemic symptoms.

BRCC3-Mediated NLRP3 Deubiquitylation Promotes Inflammasome Activation and Atherosclerosis in Clonal Hematopoiesis.

Background: Clonal hematopoiesis (CH) has emerged as an independent risk factor for atherosclerotic cardiovascular disease, with activation of macrophage inflammasomes as a potential underlying mechanism. The NLRP3 (NLR family pyrin domain containing 3) inflammasome has a key role in promoting atherosclerosis in mouse models of CH, whereas inhibition of the inflammasome product interleukin-1β appeared to particularly benefit patients with CH in CANTOS (Cardiovascular Risk Reduction Study [Reduction in Recurrent Major CV Disease Events]). is an epigenetic modifier that decreases promoter methylation.

Blockade of IL-6 signaling alleviates atherosclerosis in -deficient clonal hematopoiesis.

Clonal hematopoiesis (CH) increases the risk of atherosclerotic cardiovascular disease possibly due to increased plaque inflammation. Human studies suggest that limitation of interleukin-6 (IL-6) signaling could be beneficial in people with large CH clones, particularly in CH. Here we show that IL-6 receptor antibody treatment reverses the atherosclerosis promoted by CH, with reduction of monocytosis, lesional macrophage burden and macrophage colony-stimulating factor 1 receptor (CSF1R) expression.

External validation of the PATHFx decision-support tool on Turkish patients with skeletal metastasis.

Objective: Accurate determination of life expectancy becomes very important when determining the treatment of patients with pathologic fractures. We aimed to investigate the predictive role of the PATHFx model in Turkish patients by estimating the area under curve (AUC) of the receiver operator characteristic (ROC) and externally validating the results of PATHFx on the Turkish population.

Methods: The data of 122 patients who presented to one of four orthopaedic oncology referral centres in Istanbul (2010-2017) and underwent surgical management of pathologic fractures were retrospectively collected.

Cholesterol accumulation in macrophages drives NETosis in atherosclerotic plaques via IL-1β secretion.

Aims: Neutrophil extracellular trap formation (NETosis) increases atherosclerotic plaque vulnerability and athero-thrombosis. However, mechanisms promoting NETosis during atherogenesis are poorly understood. We have shown that cholesterol accumulation due to myeloid cell deficiency of the cholesterol transporters ATP Binding Cassette A1 and G1 (ABCA1/G1) promotes NLRP3 inflammasome activation in macrophages and neutrophils and induces prominent NETosis in atherosclerotic plaques.

Globalizing 'science and religion': examples from the late Ottoman Empire.

This article brings together insights from efforts to develop a global history of science and recent historical and sociological studies on the relations between science and religion. Using the case of the late Ottoman Empire as an example, it argues that 'science and religion' can be seen as a debate that travelled globally in the nineteenth century, generating new conceptualizations of both science and religion in many parts of the world. In their efforts to counter arguments that represented Islam as the enemy of science and progress, young Ottoman intellectuals wrote many texts addressing a specific European author, or an imagined, broad European audience in the mid- to late nineteenth century.

Erythroid lineage Jak2V617F expression promotes atherosclerosis through erythrophagocytosis and macrophage ferroptosis.

Elevated hematocrit is associated with cardiovascular risk; however, the causality and mechanisms are unclear. The JAK2V617F (Jak2VF) mutation increases cardiovascular risk in myeloproliferative disorders and in clonal hematopoiesis. Jak2VF mice with elevated WBCs, platelets, and RBCs display accelerated atherosclerosis and macrophage erythrophagocytosis.

Kindred fatalisms: debating science, Islam, and free will in the Darwinian era.

An important aspect of the nineteenth century debate on the relationship between science and religion concerned the popularity of deterministic views among scientists. An integral part of Comte's positivism, the idea of immutable laws that determined natural and social phenomena became an increasingly prevalent component of scientific perspectives in the Darwinian era. Referring to this tendency as 'scientific fatalism,' critics likened it to Calvinist predestination, which transformed the debate into one involving polemics about different branches of Christianity as well.

Myeloid LXR (Liver X Receptor) Deficiency Induces Inflammatory Gene Expression in Foamy Macrophages and Accelerates Atherosclerosis.

Background: Cholesterol loaded macrophage foam cells are a prominent feature of atherosclerotic plaques. Single-cell RNA sequencing has identified foam cells as TREM2 (triggering receptor expressed on myeloid cells 2) positive populations with low expression of inflammatory genes, resembling the TREM2 positive microglia of neurodegenerative diseases. Cholesterol loading of macrophages in vitro results in activation of LXR (liver X receptor) transcription factors and suppression of inflammatory genes.

Frequency of Congenital Aortic Arch Anomaly in COVID-19 Patients.

Objective: The aim of this study was to investigate the frequency of aortic arch anomaly in COVID-19 patients and to determine whether it will be included in the risk classification.

Methods: The study was retrospectively conducted in a third-level hospital by scanning the contrast-enhanced thoracic computed tomography and thoracic computed tomography angiography examinations of patients who received PCR (+), hospitalization, and known COVID pneumonia between March 2020 and July 2021. The study consists of 88 cases and 88 control groups.

Modulation of the NLRP3 inflammasome by Sars-CoV-2 Envelope protein.

Despite the initial success of some drugs and vaccines targeting COVID-19, understanding the mechanism underlying SARS-CoV-2 disease pathogenesis remains crucial for the development of further approaches to treatment. Some patients with severe Covid-19 experience a cytokine storm and display evidence of inflammasome activation leading to increased levels of IL-1β and IL-18; however, other reports have suggested reduced inflammatory responses to Sars-Cov-2. In this study we have examined the effects of the Sars-Cov-2 envelope (E) protein, a virulence factor in coronaviruses, on inflammasome activation and pulmonary inflammation.

Oxidized Phospholipids Promote NETosis and Arterial Thrombosis in LNK(SH2B3) Deficiency.

Background: LNK/SH2B3 inhibits Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling by hematopoietic cytokine receptors. Genome-wide association studies have shown association of a common single nucleotide polymorphism in (R262W, T allele) with neutrophilia, thrombocytosis, and coronary artery disease. We have shown that ) reduces LNK function and that LNK-deficient mice display prominent platelet-neutrophil aggregates, accelerated atherosclerosis, and thrombosis.

Posttranscriptional Regulation of the Human LDL Receptor by the U2-Spliceosome.

Background: The LDLR (low-density lipoprotein receptor) in the liver is the major determinant of LDL-cholesterol levels in human plasma. The discovery of genes that regulate the activity of LDLR helps to identify pathomechanisms of hypercholesterolemia and novel therapeutic targets against atherosclerotic cardiovascular disease.

Methods: We performed a genome-wide RNA interference screen for genes limiting the uptake of fluorescent LDL into Huh-7 hepatocarcinoma cells.

Apolipoprotein M and Sphingosine-1-Phosphate Receptor 1 Promote the Transendothelial Transport of High-Density Lipoprotein.

Objective: ApoM enriches S1P (sphingosine-1-phosphate) within HDL (high-density lipoproteins) and facilitates the activation of the S1P1 (S1P receptor type 1) by S1P, thereby preserving endothelial barrier function. Many protective functions exerted by HDL in extravascular tissues raise the question of how S1P regulates transendothelial HDL transport. Approach and Results: HDL were isolated from plasma of wild-type mice, Apom knockout mice, human apoM transgenic mice or humans and radioiodinated to trace its binding, association, and transport by bovine or human aortic endothelial cells.

The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis.

Clonal haematopoiesis, which is highly prevalent in older individuals, arises from somatic mutations that endow a proliferative advantage to haematopoietic cells. Clonal haematopoiesis increases the risk of myocardial infarction and stroke independently of traditional risk factors. Among the common genetic variants that give rise to clonal haematopoiesis, the JAK2 (JAK2) mutation, which increases JAK-STAT signalling, occurs at a younger age and imparts the strongest risk of premature coronary heart disease.