This paper reports on the occurrence, biosynthesis, metabolism, biological and toxicological profile, and assessment of the authenticity of linalool. The main biological properties of linalool – sedative, anxiolytic, analgesic, anticonvulsant, anti‐inflammatory, local anaesthetic – are discussed in terms of the molecule's chirality influence, the mechanisms of activity and type of study (in vitro, in vivo, clinical studies). Also, there is a discussion of the recent data on the skin sensitizing potential of linalool based on numerous scientific studies which have been performed in the last few years. Comments of the authenticity assessment of linalool are made considering the limitations imposed by the chemical structure, vegetal matrix or processing methods, but also from the perspective of the powerful and sophisticated analytical techniques available today (GC‐C‐IRMS, enantio‐MDGC coupled to GC‐C‐IRMS, SNIF‐NMR). Copyright © 2014 John Wiley & Sons, Ltd.
Anethole is the main fragrance and bioactive compound of anise, fennel, and star anise spices and more than other 20 plant species. It is widely used as flavor agent in food industry and other industries, in cosmetics, perfumery, and pharmaceuticals. In the last few years, various studies have revealed multiple beneficial effects of anethole for human health, such as anti-inflammatory, anticarcinogenic and chemopreventive, antidiabetic, immunomodulatory, neuroprotective, or antithrombotic, that are mediated by the modulation of several cell signaling pathways, mainly NF-kB and TNF-α signaling, and various ion channels. This chapter aims to review the scientific data and attempts to provide an insight into pharmacological activity of anethole and its therapeutic potential in human chronic diseases.
Cocoa is a rich source of high-quality antioxidant polyphenols. They comprise mainly catechins (29%–38% of total polyphenols), anthocyanins (4% of total polyphenols) and proanthocyanidins (58%–65% of total polyphenols). A growing body of experimental and epidemiological evidence highlights that the intake of cocoa polyphenols may reduce the risk of cardiovascular events. Beyond antioxidant properties, cocoa polyphenols exert blood pressure lowering activity, antiplatelet, anti-inflammatory, metabolic and anti-atherosclerotic effects, and also improve endothelial function. This paper reviews the role of cocoa polyphenols in cardiovascular protection, with a special focus on mechanisms of action, clinical relevance and correlation between antioxidant activity and cardiovascular health.
The increasing incidence of coronavirus disease 19 (COVID-19) and its polymorphic clinical manifestations due to local and systemic inflammation represent a high burden for many public health systems. Multiple evidence revealed the interdependence between the presence of cardiovascular comorbidities and a severe course of COVID-19, with heart failure (HF) being incriminated as an independent predictor of mortality. Suppression of tumorigenicity-2 ST2 has emerged as one of the most promising biomarkers in assessing the evolution and prognosis of patients with HF. The uniqueness of ST2 is determined by its structural particularities. Its transmembrane isoform exerts cardioprotective effects, while the soluble isoform (sST2), which is detectable in serum, is associated with myocardial fibrosis and poor outcome in patients with HF. Some recent data also suggested the potential role of sST2 as a marker of inflammation, while other studies highlighted it as a valuable prognostic factor in patients with COVID-19. In this review, we summarized the pathways by which sST2 is related to myocardial injury and its connection to the severity of inflammation in patients with COVID-19. Also, we reviewed possible perspectives of using it as a dual cardio-inflammatory biomarker, for both early diagnosis, risk stratification and prognosis assessment of patients with concomitant HF and COVID-19.
(1) Background: There are limited clinical data in patients from the Eastern European regions hospitalized for a severe form of Coronavirus disease 2019 (COVID-19). This study aims to identify risk factors associated with intra-hospital mortality in patients with COVID-19 severe pneumonia admitted to a tertiary center in Iasi, Romania. (2) Methods: The study is of a unicentric retrospective observational type and includes 150 patients with severe COVID-19 pneumonia divided into two subgroups, survivors and non-survivors. Demographic and clinical parameters, as well as comorbidities, laboratory and imaging investigations upon admission, treatments, and evolution during hospitalization were recorded. First, we sought to identify the risk factors associated with intra-hospital mortality using logistic regression. Secondly, we assessed the correlations between D-Dimer and C-reactive protein and predictors of poor prognosis. (3) Results: The predictors of in-hospital mortality identified in the study are D-dimers >0.5 mg/L (p = 0.002), C-reactive protein >5mg/L (p = 0.001), and heart rate above 100 beats per minute (p = 0.001). The biomarkers were also significantly correlated the need for mechanical ventilation, admission to intensive care unit, or multiple organ dysfunction syndrome. By area under the curve (AUC) analysis, we noticed that both D-Dimer (AUC 0.741) and C-reactive protein (AUC 0.707) exhibit adequate performance in predicting a poor prognosis in patients with severe viral infection. (4) Conclusions: COVID-19′s outcome is significantly influenced by several laboratory and clinical factors. As mortality induced by severe COVID-19 pneumonia is considerable, the identification of risk factors associated with negative outcome coupled with an early therapeutic approach are of paramount importance, as they may significantly improve the outcome and survival rates.
The close connection and interaction between the cardiac and the liver functions are well-known, as cirrhotic cardiomyopathy is an important clinical entity which best describes the mutual pathogenical influence between these two organs. Due to the fact that cardiac dysfunction in patients with chronic hepatic disorders is oligosymptomatic or even asymptomatic, an early diagnosis represents a challenge for every physician. Syndecan-1—a transmembrane proteoglycan that exerts its functions mainly via its heparane sulfate chains—is a very promising biomarker, correlated not only with the degree of cardiac fibrosis but also with the severity of liver fibrosis. Many studies highlighted its role in the development of cardiac fibrosis or atherogenesis, being significantly correlated with the activity of angiotensin II. Multiple evidence revealed that syndecan-1 is also associated with tissue injury and may regulate inflammatory and regenerative responses, being considered a protective molecule that limits the inflammation and reduces cardiac remodelling and dysfunction after a myocardial infarction. Syndecan-1 may also be used as a reliable biomarker for the noninvasive assessment of liver fibrosis. Under various fibrogenetic conditions, shedding of syndecan's extracellular domain took place, becoming a soluble form that binds different growth factors and inhibits further fibrosis. This complex molecule is also involved in the lipid metabolism, by altering the clearance of cholesterol particles, and in chronic hepatitis, by enhancing the viral invasion of hepatocytes. Due to the growing interest in this biomarker, multiple studies aimed at revealing syndecan-1's potential benefits in the diagnosis and prognosis assessment in patients with heart failure or chronic liver disorders. In this review, we review the mechanisms by which syndecan-1 exerts its effects and the possible perspectives opened by its use as a dual cardio-hepatic biomarker.
The incidence of urinary tract infections (UTIs) caused by Klebsiella pneumoniae has exhibited an increasing trend and has become a high burden for many public health systems, especially in hospital settings. Multidrug resistance associated with the production of extended-spectrum β-lactamases (ESBL) among K. pneumoniae isolates is endemic in Southeastern Europe. We retrospectively analyzed 75 cases admitted to 'St. Parascheva' Clinical Hospital of Infectious Diseases in Iasi, Romania, during the first 6 months of 2019 (January 1 to June 30), who had a confirmed diagnosis of K. pneumoniae UTI at discharge. From a total of 75 patients, 34 (45.3%) presented ESBL + K. pneumoniae. The mean age was 66 years (70.1 for the ESBL + patients vs. 62.6 for the ESBLpatients, P=0.0365). There was a symmetrical sex distribution (37 men vs. 38 women). Of these, 22 men had ESBL + K. pneumoniae UTIs, compared to only 15 with an ESBLstrain, P=0.0087. Another risk factor for ESBL + K. pneumoniae UTIs was the presence of hospitalization in the past 6 months; 20 (58.82%) patients with ESBL + infections were previously hospitalized, compared to only 5 (12.19%) patients with ESBLstrains, P<0.0001. The urinary catheter carriers presented an increased prevalence of ESBL + infections (15/34 vs. 5/41, P=0.0012). Regarding mortality, ESBL + infections caused 6 fatalities, compared to only 1 death in the ESBLgroup, P=0.0166. ESBL + K. pneumoniae strains represent an important cause of healthcare-related UTIs, with a significantly higher mortality rate compared to ESBLstrains. Early identification and adequate management of the risk factors incriminated in ESBL + UTIs should be a priority for physicians in order to limit the dissemination of the ESBL-producing strains and thus to improve the outcome of these patients.
In the modern era, coronary artery disease (CAD) has become the most common form of heart disease and, due to the severity of its clinical manifestations and its acute complications, is a major cause of morbidity and mortality worldwide. The phenotypic variability of CAD is correlated with the complex etiology, multifactorial (caused by the interaction of genetic and environmental factors) but also monogenic. The purpose of this review is to present the genetic factors involved in the etiology of CAD and their relationship to the pathogenic mechanisms of the disease. Method: we analyzed data from the literature, starting with candidate gene-based association studies, then continuing with extensive association studies such as Genome-Wide Association Studies (GWAS) and Whole Exome Sequencing (WES). The results of these studies revealed that the number of genetic factors involved in CAD etiology is impressive. The identification of new genetic factors through GWASs offers new perspectives on understanding the complex pathophysiological mechanisms that determine CAD. In conclusion, deciphering the genetic architecture of CAD by extended genomic analysis (GWAS/WES) will establish new therapeutic targets and lead to the development of new treatments. The identification of individuals at high risk for CAD using polygenic risk scores (PRS) will allow early prophylactic measures and personalized therapy to improve their prognosis.
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