Metabolomics:Open Access

In the event of an intentional or accidental release of ionizing radiation in a densely populated area, timely assessment and triage of the general population for radiation exposure is critical. Despite decades of research, counter measures still lack. In this study, we describe the potential of integrated NMR and LC-MS approaches in evaluating the radiation biomarkers. Untargeted profiling by means of broad-spectrum, highly sensitive, UPLC-ESI-QTOFMS provides a comprehensive list of metabolites at one go in a single biofluid.

For the emergence of life, the origin of metabolism stands as a central problem. How did early biomolecules arise to form an intertwined network of self-controlling metabolic reactions? In scenarios for a potential chemoautotrophic origin of life, the relevant conditions could involve volcanic discharges and ashes or gradients in volcanic hydrothermal vents.

The etiology and pathogenesis of Hirschsprung’s disease (HSCR) remain largely unknown. Here we employed a multiple ‘omics’-analysis to explore the important pathway related to the development of HSCR. We examined colon tissues from three independent populations with a combined analysis of metabolomics, transcriptomics and proteomics to understand HSCR. Mouse model was used for examining PGE2 induced clinical presentation of HSCR. SH-SY5Y and SK-NBE(2) cell lines were used for examining PGE2 inhibited cell migration through EP2.

Quantitative assessment of disease activity
is important for effective disease management in
Takayasu arteritis (TA) which is an immune-mediated
inflammatory disease. The dominance of oxidative stress
is the hallmark of active inflammation. Both clinical and
preclinical data suggest that histidine has its strong antioxidative
and anti-inflammatory effects [1,2]. Based on
this, we hypothesized that the circulatory Histidine can
serve as an indicant of active inflammation and so for
monitoring disease activity in TA.

Troglitazone (TGZ) is a member of thiazolidinedione class of chemicals was developed for the treatment of type 2 diabetes in the late 1990s. TGZ was withdrawn from the market in 2000 due to a number of fatalities due incidence of idiosyncratic liver toxicity. Till date, the mechanism of TGZ-induced liver toxicity is unclear. However, several molecular mechanisms have been proposed to underlie TGZs liver toxicity. Understanding the interactions between these mechanisms could aid drug developers more robustly predict drug-induced liver injury (DILI), a major cause of drug withdrawal.