We provided the phenotype and marker genes of IVD cells at the single-cell level, reconfirmed existing data, and proposed new marker genes, including MSC marker genes. By identifying more accurate target cells and genes, our results pave the way for further study of the response of individual disc cells to disease states and provide the basis for future disc regeneration therapies.

We provided the phenotype and marker genes of IVD cells at the single-cell level, reconfirmed existing data, and proposed new marker genes, including MSC marker genes. By identifying more accurate target cells and genes, our results pave the way for further study of the response of individual disc cells to disease states and provide the basis for future disc regeneration therapies.

The reported association between an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene and the risk for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) remains controversial despite the publication of four meta-analyses on this topic. Here, we updated the meta-analysis with more studies and additional assessments that include adults and children within the context of the coronavirus disease 2019 (COVID-19) pandemic.

Sixteen articles (22 studies) were included. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using three genetic models (allele, recessive and dominant), in which ARDS patients were compared with non-ARDS patients (A1) and healthy controls (A2). Mortality outcomes were also assessed (A3). The influence of covariates was examined by meta-regression. Bonferroni correction was performed for multiple pooled associations. Subgroup analyses based on ethnicity (Asians, Caucasians) and life stage (adults, children) were conducteOVID-19.

Significant associations of the ACE I/D polymorphism with the risk of ALI/ARDS were indicated in Caucasians and children as well as in Asians in mortality analysis. These findings were underpinned by high significance, high statistical power and robustness. ACE genotypes may be useful for ALI/ARDS therapy for patients with COVID-19.Atrial fibrillation (AF) is a common arrhythmia that can lead to stroke. The diseased muscle tissue of the atria develops atrial fibrosis, inflammation, thrombosis and subsequent strokes, resulting in significant morbidity and mortality. Current diagnostic and evaluation paradigms for clinical AF focus on identifying functional and morphological abnormalities of the left atria by echocardiography. Notably, the development of atrial substrate that marks AF likely occurs for years before the manifestation of AF onset, meaning that the functional and morphometrical aberrations are end-stage features, representing a stable state of an already-compromised tissue. There is no existing ‘gold standard’ measure to identify the early atrial muscle disease and characterization of the atrial substrate is inadequate. In fact, sub-clinical identification of atrial myopathy is not undertaken in clinical practice because there is no robust screening method. Development of molecular imaging probes for detection of atrial muscle disease might enable early detection and staging of AF, ultimately leading to improved treatment outcome. In this review, we discuss possible molecular imaging targets that may enable early diagnosis of cardiovascular disease, with focus on novel insights, challenges and opportunities for sub-clinical imaging of atrial myopathy and AF.As the prevalence of asymptomatic COVID-19 continues to increase, there is an increasing possibility that patients with COVID-19 may presen with ST-segment elevation myocardial infarction (STEMI). With social distancing and restricted access to preventive healthcare and emergency services, the management of acute cardiac emergencies such as myocardial infarction has suffered collateral damage. Thus far, global trends suggest a decrease in STEMI activations with possible worse outcomes due to delayed presentation and management. In this review, we discuss the challenges to STEMI management in the COVID-19 era and provide potential solutions for adherence to evidence-based therapies as the pandemic progresses into the year 2021.Coronavirus disease of 2019 (COVID-19) is the respiratory viral infection caused by the coronavirus SARS-CoV2 (Severe Acute Respiratory Syndrome Coronavirus 2). Despite being a respiratory illness, COVID-19 is found to increase the risk of venous and arterial thromboembolic events. Indeed, the link between COVID-19 and thrombosis is attracting attention from the broad scientific community. In this review we will analyze the current available knowledge of the association between COVID-19 and thrombosis. MK-0859 mouse We will highlight mechanisms at both molecular and cellular levels that may explain this association. In addition, the article will review the antithrombotic properties of agents currently utilized or being studied in COVID-19 management. Finally, we will discuss current professional association guidance on prevention and treatment of thromboembolism associated with COVID-19.The quinone derivative of the non-psychotropic cannabinoid cannabigerol (CBG), so-called VCE-003.2, has been recently investigated for its neuroprotective properties in inflammatory models of Parkinson’s disease (PD) in mice. Such potential derives from its activity at the peroxisome proliferator-activated receptor-γ (PPAR-γ). In the present study, we investigated the neuroprotective properties of VCE-003.2 against the parkinsonian neurotoxin 6-hydroxydopamine (6-OHDA), in comparison with two new CBG-related derivatives, the cannabigerolic acid quinone (CBGA-Q) and its sodium salt CBGA-Q-Salt, which, similarly to VCE-003.2, were found to be active at the PPAR-γ receptor, but not at the cannabinoid CB1 and CB2 receptors. First, we investigated their cytoprotective properties in vitro by analyzing cell survival in cultured SH-SY5Y cells exposed to 6-OHDA. We found an important cytoprotective effect of VCE-003.2 at a concentration of 20 μM, which was not reversed by the blockade of PPAR-γ receptors with GW9662, supporting its activity at an alternative site (non-sensitive to classic antagonists) in this receptor.