A Systematic Review and Meta-analysis to Identify Risk Factors for Developing Long COVID-19.

Aim: This systematic review and meta-analysis was undertaken to identify the risk factors of long coronavirus disease 2019 (COVID-19) to provide insight for selecting cases for more aggressive monitoring and treatment after COVID-19 infection and reduce morbidity due to long COVID-19.

Materials And Methods: All relevant studies published till July 2022 were searched for in PubMed, Trip database, and the Cochrane Central Register of Controlled Trials (CENTRAL; The Cochrane Library). Reference lists of the studies selected for appraisal were also considered.

Characteristics and Outcomes of COVID-19 during the Third Wave of COVID Pandemic: A Single-center Descriptive Study.

Aim: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has been causing a global pandemic of Coronavirus (COVID-19) disease in recurring waves. On November 24, 2021, a new SARS-CoV-2 variant (B.1.

Neurological Manifestations and Their Effect on Outcome in Second Wave of COVID-19 Pandemic: A Retrospective Cohort Study.

Aim: There is a need for a better understanding of the relation of various neurological symptoms and complications with manifestations and outcomes of coronavirus disease 2019 (COVID-19). Hence, we planned this study to get an insight into the relation of neurological manifestations and COVID-19.

Materials And Methods: This was a retrospective study.

Cross-talk between inflammation and angiotensin II: studies based on direct transfection of cardiomyocytes with AT1R and AT2R cDNA.

Ischemic myocardium exhibits inflammation, local angiotensin II (Ang II) generation and up-regulation of LOX-1, a lectin-like ox-LDL receptor. To define the inter-active roles of Ang II and inflammation in furthering tissue injury, cultured HL-1 cardiomyocytes were treated with Ang II. Ang II treatment up-regulated the expression of Ang II type 1 (AT1R) and type 2 (AT2R) receptors as well as LOX-1.

Myocardial protection during off pump coronary artery bypass surgery: a comparison of inhalational anesthesia with sevoflurane or desflurane and total intravenous anesthesia.

Aims And Objectives: The objective of the study was to evaluate the myocardial protective effect of volatile agents-sevoflurane and desflurane versus total intravenous anesthesia (TIVA) with propofol in offpump coronary artery bypass surgery (OPCAB) by measuring cardiac troponin-T (cTnT) as a marker of myocardial cell death.

Materials And Methods: The study was conducted on 139 patients scheduled to undergo elective OPCAB surgery. The patients were randomly allocated to receive anesthesia with sevoflurane, desflurane or TIVA with propofol.

Large impact of low concentration oxidized LDL on angiogenic potential of human endothelial cells: a microarray study.

Oxidized LDL (ox-LDL) is a key factor in atherogenesis. It is taken up by endothelial cells primarily by ox-LDL receptor-1 (LOX-1). To elucidate transcriptional responses, we performed microarray analysis on human coronary artery endothelial cells (HCAECs) exposed to small physiologic concentration of ox-LDL- 5 µg/ml for 2 and 12 hours.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) and cardiac fibroblast growth.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) regulates growth of a variety of cells and is important in inflammation, oxidative stress, and tissue remodeling. Recent studies show that LOX-1 deletion limits cardiac remodeling after sustained hypertension. We posited that LOX-1 may affect cardiac fibroblast growth and collagen secretion.

Aspirin inhibits oxidant stress, reduces age-associated functional declines, and extends lifespan of Caenorhabditis elegans.

Aims: Oxidative stress and inflammation are leading risk factors for age-associated functional declines. We assessed aspirin effects on endogenous oxidative-stress levels, lifespan, and age-related functional declines, in the nematode Caenorhabditis elegans.

Results: Both aspirin and its salicylate moiety, at nontoxic concentrations (0.

Outcomes of in-hospital, out of intensive care and operation theatre cardiac arrests in a tertiary referral hospital.

Objective: Cardiac arrest in the hospital wards may not receive as much attention as it does in the operation theatre and intensive care unit (ICU). The experience and the qualifications of personnel in the ward may not be comparable to those in the other vital areas of the hospital. The outcome of cardiac arrest from the ward areas is a reasonable surrogate of training of the ward nurses and technicians in cardiopulmonary resuscitation.

Aspirin downregulates angiotensin type 1 receptor transcription implications in capillary formation from endothelial cells.

Aspirin [acetyl salicylic acid (ASA)] inhibits nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and reactive oxygen species generation, a pathway that underlies formation of new capillaries (angiogenesis). Angiotensin II (Ang II) participates in angiogenesis by activating type 1 receptor (AT1R). We examined if ASA would inhibit AT1R transcription, which requires NADPH oxidase, and thereby new capillary formation.

Delineation of the effects of angiotensin type 1 and 2 receptors on HL-1 cardiomyocyte apoptosis.

Angiotensin II (Ang II) exerts its effects by activating its receptors, primarily type 1 (AT1R) and type 2 (AT2R). While the role of AT1R activation in cardiomyocyte physiology is well known, the role of AT2R in cardiomyocyte apoptosis remains controversial. To define the precise role of AT1R and AT2R in this process, we transfected HL-1 cardiomyocytes with AT1R or AT2R cDNA, and examined markers of apoptosis.

A randomized prospective analysis of alteration of hemostatic function in patients receiving tranexamic acid and hydroxyethyl starch (130/0.4) undergoing off pump coronary artery bypass surgery.

Postoperative hemorrhagic complications is still one of the major problems in cardiac surgeries. It may be caused by surgical issues, coagulopathy caused by the side effects of the intravenous fluids administered to produce plasma volume expansion such as hydroxyl ethyl starch (HES). In order to thwart this hemorrhagic issue, few agents are available.

Aspirin suppresses cardiac fibroblast proliferation and collagen formation through downregulation of angiotensin type 1 receptor transcription.

Aspirin (acetyl salicylic acid, ASA) is a common drug used for its analgesic and antipyretic effects. Recent studies show that ASA not only blocks cyclooxygenase, but also inhibits NADPH oxidase and resultant reactive oxygen species (ROS) generation, a pathway that underlies pathogenesis of several ailments, including hypertension and tissue remodeling after injury. In these disease states, angiotensin II (Ang II) activates NADPH oxidase via its type 1 receptor (AT1R) and leads to fibroblast growth and collagen synthesis.

Current Concepts of the Role of Oxidized LDL Receptors in Atherosclerosis.

Atherosclerosis is characterized by accumulation of lipids and inflammatory cells in the arterial wall. Oxidized low-density lipoprotein (ox-LDL) plays important role in the genesis and progression of atheromatous plaque. Various scavenger receptors have been recognized in the past two decades that mediate uptake of ox-LDL leading to formation of foam cells.

Adherence junction proteins in angiogenesis: modulation by aspirin and salicylic acid.

Background: The development of neovasculature correlates with plaque instability and rupture as well as tumor growth and aggressiveness. In recent years, aspirin has emerged as a powerful modality in prophylaxis of cardiovascular events, which may be linked to its inhibitory effects on angiogenesis.

Methods And Results: We studied the role of endothelial adherens junctions in angiogenesis and the modulation of adherens junctions by acetylsalicylic acid (ASA) and salicylic acid as mechanisms of the angiostatic potential of these agents.

Oxidized LDL, LOX-1 and atherosclerosis.

An elevated level of low density lipoprotein (LDL) cholesterol constitutes a major risk factor for genesis of atherosclerosis. Ox-LDL plays a more important role in the genesis and progression of atherosclerosis than the native LDL. Ox-LDL leads to endothelial dysfunction leading to expression of adhesion molecules and recruitment of monocyte in subendothelial space.

LOX-1: a new target for therapy for cardiovascular diseases.

There is much interest in the role of oxidant stress in an ever-increasing list of disease states. However, the precise mediator of oxidant stress and the stressor molecule/s have not been identified. Accordingly, trials of inhibitors of oxidant stress in animal models of disease states have met only limited success.

Oxidized low-density lipoprotein and atherosclerosis implications in antioxidant therapy.

Low-density lipoprotein (LDL)-cholesterol is important for cellular function, but in high concentrations, it can lead to atheroma formation. Over the past several decades, it has become abundantly evident that the oxidized form of LDL-cholesterol (ox-LDL) is more important in the genesis and progression of atherosclerosis than native unmodified LDL-cholesterol. Ox-LDL leads to endothelial dysfunction, an initial step in the formation of an atheroma.

Oxidized LDL receptor 1 (OLR1) as a possible link between obesity, dyslipidemia and cancer.

Recent studies have linked expression of lectin-like ox-LDL receptor 1 (OLR1) to tumorigenesis. We analyzed microarray data from Olr1 knockout (KO) and wild type (WT) mice for genes involved in cellular transformation and evaluated effects of OLR1 over-expression in normal mammary epithelial cells (MCF10A) and breast cancer cells (HCC1143) in terms of gene expression, migration, adhesion and transendothelial migration. Twenty-six out of 238 genes were inhibited in tissues of OLR1 KO mice; the vast majority of OLR1 sensitive genes contained NF-κB binding sites in their promoters.

Prior exposure to oxidized low-density lipoprotein limits apoptosis in subsequent generations of endothelial cells by altering promoter methylation.

Oxidized LDL (ox-LDL) plays a critical role in atherogenesis, including apoptosis. As hypercholesterolemia causes epigenetic changes resulting in long-term phenotypic consequences, we hypothesized that repeated and continuous exposure to ox-LDL may alter the pattern of apoptosis in human umbilical vein endothelial cells (HUVECs). We also analyzed global and promoter-specific methylation of apoptosis-related genes.

Oxidative stress and lectin-like ox-LDL-receptor LOX-1 in atherogenesis and tumorigenesis.

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) has been identified as a major receptor for oxidized low-density lipoprotein (ox-LDL) in endothelial cells, monocytes, platelets, cardiomyocytes, and vascular smooth muscle cells. Its expression is minimal under physiological conditions but can be induced under pathological conditions. The upregulation of LOX-1 by ox-LDL appears to be important for physiologic processes, such as endothelial cell proliferation, apoptosis, and endothelium remodeling.

Angiostatic effects of aspirin in hypoxia-reoxygenation are linked to modulation of TGFβ1 signaling.

Hypoxia-reoxygenation (HR) is a major driver for angiogenesis in atherosclerotic plaques and tumors. Angiogenesis is a multistep process requiring stimulation of proliferation and migration of endothelial cells in response to a number of growth factors, including transforming growth factor (TGFβ1). Aspirin (acetylsalicylic acid) has been shown to reduce atherosclerosis-related events as well as development of certain tumors.

Antiangiogenic and antimitotic effects of aspirin in hypoxia–reoxygenation modulation of the LOX-1-NADPH oxidase axis as a potential mechanism.

Hypoxia–reoxygenation (HR) is a primary driver of angiogenesis in both atherogenesis and tumorigenesis. The main target of hypoxia-driven proangiogenic signaling is adherens junctions responsible for contact inhibition of endothelial cells. We analyzed the effects of hypoxia (8–12 hours) followed by a brief period of reoxygenation (2 hours) (HR) on angiogenesis and integrity of adherens junction in cultured human umbilical vein endothelial cells as well as the effects of aspirin on modulation of human umbilical vein endothelial cells' response to HR.