OBJECTIVE Flavocoxid is a prescription medical food used to manage osteoarthritis (OA) symptoms. Safety concerns based on case reports raised an association with acute liver injury and hypersensitivity pneumonitis. We determined incidence rates (IR) of these safety events in a cohort of new users of flavocoxid and prescription non-steroidal anti-inflammatory drugs (NSAIDs). METHOD MarketScan claims data (2006-2017) was used to identify patients initiating flavocoxid or NSAIDs. Propensity score matching (12 ratio) was used to balance patient characteristics. Outcomes included hospitalization for hypersensitivity pneumonitis, liver injury, gastrointestinal bleeding, myocardial infarction, and acute kidney injury. Poisson regression was used to calculate IRs and Cox regression for calculating adjusted hazard ratios (aHR). RESULTS 3,337 flavocoxid and 6,674 NSAID users met eligibility criteria. Before matching, flavocoxid users were older (mean 57 vs 51 years), had more polypharmacy (68% vs 29% taking ≥11 medications). After matching, characteristics were well balanced. The rate of hypersensitivity pneumonitis was 1.1 (95%CI 0.0-5.9) per 1,000 PY for flavocoxid and 0.0 (95%CI 0.0-2.2) for NSAIDs. For hospitalized liver injury, it was 3.2 (95%CI 0.7-9.3) for flavocoxid and 2.4 (95%CI 0.7-6.1) for NSAIDs, aHR = 1.16, 95%CI 0.23-6.01. A lower rate of GI bleed was observed, IR 5.3 (1.7-12.3) for flavocoxid and 10.2 (5.9-16.3) for NSAIDs, aHR 0.49(0.18-1.68). There were no significant differences for MI or AKI. CONCLUSION The rate of hypersensitivity pneumonitis and liver injury associated with flavocoxid was low and minimally elevated compared to NSAIDs. Flavocoxid users had a significantly lower risk for hospitalized GI bleeding. The risk-benefit profile of flavocoxid may warrant reevaluation in light of these findings. Preclinical imaging in osteoarthritis is a rapidly growing area with three principal objectives to provide rapid, sensitive tools to monitor the course of experimental OA longitudinally; to describe the temporal relationship between tissue-specific pathologies over the course of disease; and to use molecular probes to measure disease activity in vivo. Research in this area can be broadly divided into those techniques that monitor structural changes in tissues (microCT, microMRI, ultrasound) and those that detect molecular disease activity (positron emission tomography (PET), optical and optoacoustic imaging). The former techniques have largely evolved from experience in human joint imaging and have been refined for small animal use. Some of the latter tools, such as optical imaging, have been developed in preclinical models and may have translational benefit in the future for patient stratification and for monitoring disease progression and response to treatment. In this narrative review we describe these methodologies and discuss the benefits to animal research, understanding OA pathogenesis, and in the development of human biomarkers. Impaired vascularization of adipose tissue leads to local hypoxia and results in chronic inflammation and obesity-related metabolic disorders. We have recently constructed an engineered protein named tPep-VEGF-B by bridging vascular endothelial growth factor (VEGF-B) with an adipose-targeted peptide. Here, we reported tPep-VEGF-B diminishes obesity and alleviates metabolic syndrome. High fat diet (HFD) treated mice had reduced adipose vascular density and showed adipose hypoxia and metabolic complications. In contrast, the treatment of tPep-VEGF-B repressed HFD-induced body weight gain, which led to increased adipose vasculature and reduced hypoxia. This treatment also alleviated obesity associated hyperlipidemia and fatty liver disease. This study provided a leading molecule for the treatment of type 2 diabetes and other metabolic diseases. It also provided experimental support for the theory that modulation of angiogenesis plays a key role in the treatment of metabolic diseases. AIMS To investigate the effect of lncRNA LCTS5 in the non-small cell lung cancer (NSCLC). MATERIALS AND METHODS LncRNA profiling was used to identify the novel lncRNA LCTS5. Viability and migration assays were implemented to evaluate the in vitro effect of LCTS5. Transplantation study was designed to investigate the in vivo role. Short hairpin RNA (shRNA) and lentiviral vector were used to alter LCTS5 expression. KEY FINDINGS We identified a novel lncRNA named LCTS5 whose abundance is dramatically decreased in NSCLC. Overexpressing LCTS5 effectively inhibits viability and migration. Meanwhile, LCTS5 overexpression retards xenograft tumor growth and proliferation. LCTS5 interacts with INO80 to reduce INO80 occupancy at enhancer regions of multiple lung cancer related genes without affecting INO80 decay. SIGNIFICANCE The newly identified lncRNA LCTS5 impairs NSCLC progression and provides a compelling target for therapeutic intervention during NSCLC treatments. AIMS Hydrogen sulfide (H2S) as a novel gasotransmitter can be endogenously produced in liver by cystathionine gamma-lyase (CSE). The dysfunctions of CSE/H2S system have been linked to various liver diseases. Acetyl-CoA is the key intermediate from the metabolism of lipid. This study examined the roles of H2S in hepatic acetyl-CoA and lipid metabolism. MATERIALS AND METHODS Both in vitro cell model and in vivo animal model of lipid accumulation were used in this study. Western blotting and real-time PCR were used for analysis of protein and mRNA expression. Acetyl-CoA was analyzed by a coupled enzyme assay, and lipid accumulation was observed with Oil Red O staining. KEY FINDINGS Incubation of human liver carcinoma (HepG2) cells with a mixture of free fatty acids (FFAs) or high glucose reduced CSE expression and H2S production, promoted intracellular accumulation of acetyl-CoA and lipid. Onametostat Supply of exogenous NaHS or cysteine reduced acetyl-CoA contents and lipid accumulation, while blockage of CSE activity promoted intracellular lipid accumulation. Furthermore, H2S blocked FFAs-induced transcriptions of de novo lipogenesis, inflammation, and fibrosis-related genes. In vivo, knockout of CSE gene stimulated more hepatic acetyl-CoA and lipid accumulation in mice induced by high-fat choline-deficient diet. The expressions of lipogenesis, inflammation, and fibrosis-related genes were significantly higher in liver tissues from CSE knockout mice when compared with wild-type mice. SIGNIFICANCE CSE/H2S system is indispensable for maintaining the homeostasis of acetyl-CoA and lipid accumulation and protecting from the development of inflammation and fibrosis in liver under excessive caloric ingestion.