Inhibition of platelet activation process upon tris (2-chloroethyl) phosphate exposure: Role of PFKP-mediated glycolysis and the pentose phosphate pathway.

Tris (2-chloroethyl) phosphate (TCEP), recognized as an emerging pollutant, has been frequently detected in human blood. Maintenance of blood homeostasis is indispensable for regulating various physiological states and overall health, yet hematological toxicology of TCEP has not been extensively investigated. Platelets, a vital component of blood, are fundamental in the processes of hemostasis and thrombosis through their activation; thus, this study was designed to elucidate the effects and underlying mechanisms of TCEP on platelet activation.

Cardiotoxicity of tris(2-chloroethyl) phosphate exposure: Insights into the role of oxygen sensor mediated energy metabolism remodeling.

Tris(2-chloroethyl) phosphate, an extensively used organophosphorus flame retardant in consumer products, has caused pervasive environmental contamination and increased human exposure, raising concerns about its cardiotoxic potential. However, the detailed toxicological profile, particularly concerning the crucial cardiac energy metabolism, and the precise mechanisms remain poorly understood. This study in C57BL/6 J mice exposed to TCEP for 36 days at varying doses revealed cardiac dysfunction, structural abnormalities, and hypoxia.

PFOS impairs cardiac function and energy metabolism under high-fat diet: Insights into role of circulating macrophage emphasized by exposure distribution.

Per- and polyfluoroalkyl substances (PFAS), widely utilized in consumer products, have been linked to an increased risk of cardiovascular disease (CVD). With the increasing prevalence of high-fat diet, a common risk factor for CVD, the PFAS exposed populations who consume a high-fat diet will inevitably grow and may have a higher CVD risk. However, the potential toxic effect and mode of action remain elusive.

TBBPA rather than its main derivatives enhanced growth of endometrial cancer via p53 ubiquitination.

Tetrabromobisphenol A (TBBPA) and its derivatives widely exist in various environments and biota. Although the available data indicate that TBBPA exposure is highly associated with the increased incidence of endometrial cancer (EC), the effects of TBBPA and its main derivatives on EC proliferation and the involved crucial mechanism remain unclear. The present study aimed to investigate the effects of TBBPA and its derivatives under environmental concentrations on the proliferation of EC, and the crucial mechanism on the progression of EC caused by bromine flame retardants exposure.

Oxygen sensors mediated HIF-1α accumulation and translocation: A pivotal mechanism of fine particles-exacerbated myocardial hypoxia injury.

Epidemiological studies have demonstrated a strong association of ambient fine particulate matter (PM) exposure with the increasing mortality by ischemic heart disease (IHD), but the involved mechanisms remain poorly understood. Herein, we found that the chronic exposure of real ambient PM led to the upregulation of hypoxia-inducible factor-1 alpha (HIF-1α) protein in the myocardium of mice, accompanied by obvious myocardial injury and hypertrophy. Further data from the hypoxia-ischemia cellular model indicated that PM-induced HIF-1α accumulation was responsible for the promotion of myocardial hypoxia injury.

TBBPA stimulated cell migration of endometrial cancer via the contribution of NOX-generated ROS in lieu of energy metabolism.

Due to the extensive applications and deleterious effects of Tetrabromobisphenol A (TBBPA), the health risk and possible mechanisms have been a topic of concern. However, the knowledge on carcinogenic risk of TBBPA and corresponding mechanisms remains scarce. In this study, endometrial cancer cells were exposed to low doses of TBBPA and its main derivatives including TBBPA bis (2,3-dibromopropyl ether) (TBBPA-BDBPE) and TBBPA bis (2-hydroxyethyl ether) (TBBPA-BHEE).

Critical biomarkers for myocardial damage by fine particulate matter: Focused on PPARα-regulated energy metabolism.

Fine particulate matter is one of the leading threats to cardiovascular health worldwide. The exploration of novel and sensitive biomarkers to detect damaging effect of fine particulate matter on cardiac tissues is of great importance in the better understanding of haze-caused myocardial injury. A link between heart failure and PPARα-regulated energy metabolism has been confirmed previously.

Fine particles cause the abnormality of cardiac ATP levels via PPARɑ-mediated utilization of fatty acid and glucose using in vivo and in vitro models.

Ambient fine particle (PM) is one of the potential risk factors for the cardiovascular disease, which is characterized by a marked shift in energy substrate preference leading to the reduction of adenosine triphosphate (ATP) synthesis. The metabolic adaptation is brought about by alterations in substrate transporters. Hence, this study aimed to investigate the effects and possible mechanisms of seasonal PM exposure on alteration of cardiac ATP content.

Coexisting JAK2V617F and CALR Exon 9 Mutation in Essential Thrombocythemia.

Classic "BCR-ABL1-negative" MPN is an operational sub-category of MPN that includes polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF) harboring JAK2V617F as the most common mutation. JAK2V617F can be detected in about 95 % of patients with PV while remaining 5 % of PV patients carry a somatic mutation of JAK2 exon 12. Approximately one-third of patients with ET or PMF do not carry any mutation in JAK2 or MPL.

Coexisting JAK2V617F and CALR Exon 9 Mutations in Myeloproliferative Neoplasms - Do They Designate a New Subtype?

The classic BCR-ABL1-negative myeloproliferative neoplasm is an operational sub-category of MPNs that includes polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). The JAK2V617F mutation is found in ~ 95% of PV and 50-60% of ET or PMF. In most of the remaining JAK2V617F- negative PV cases, JAK2 exon 12 mutations are present.

Characterization of high molecular weight dextran produced by Weissella cibaria CMGDEX3.

Exopolysaccharide (EPS) producing Weissella cibaria CMGDEX3 was isolated from cabbage on sucrose containing De Man, Rogosa and Sharpe (MRS) agar. Dextransucrase activity and dextran yield was found to be 7.1 DSU ml(-1) and 2.