Over 100 structural models of l-asparaginases have been deposited in the Protein Data Bank during the last 30 years. One of the prime achievements of structure-centered approaches was the elucidation of the details of the mechanism of enzymatic action of this unique hydrolase that utilizes a side chain of threonine as the primary nucleophile. The molecular basis of other important properties of these enzymes, such as their substrate specificity, is still being evaluated. Results of structural and mechanistic studies of l-asparaginases are being utilized in efforts to improve the clinical properties of this important anticancer drug.The ability of cells to convert mechanical perturbations into biochemical information is an essential aspect of mammalian physiology. The molecules that mediate such mechanotransduction include mechanically activated ion channels, which directly convert mechanical inputs into electrochemical signals. The unifying feature of these channels is that their open probability increases with the application of a mechanical input. However, the structure, activation profile and sensitivity of distinct mechanically activated ion channels vary from channel to channel. In this review, we discuss how ionic currents can be mechanically evoked and monitored in vitro, and describe the distinct activation profiles displayed by a range of mammalian channels. In addition, we discuss the various mechanisms by which the best-characterized mammalian, mechanically activated ion channel, PIEZO1, can be modulated. The diversity of activation and modulation of these mammalian ion channels suggest that these molecules may facilitate a finely controlled and diverse ability to sense mechanical inputs in mammalian cells. Study objectives were to (i) develop and test a whole-of-system method for identifying patients who meet a major trauma by-pass guideline definition; (ii) apply this method to assess conformance to the current 2006 guideline for a road trauma cohort; and (iii) leverage relevant findings to propose improvements to the guideline. Retrospective analysis of existing, routinely collected data relating to Queensland road trauma patients July 2015 to June 2017. Data from ambulance, aero-medical retrievals, ED, hospital and death registers were linked and used for analysis. Processes of care measured included frequency of pre-hospital triage criteria, distribution of destination (trauma service level), compliance with guideline (recommended vs actual destination), trauma service level by threat to life (injury severity) (all modes of transport and aero-medical in particular), proportion of patients requiring only ED, transport pathway (direct vs inter-hospital transfer). 3847 cases were identified from data as sment of conformance to guideline and future revision of the thresholds. Bolus tracking is applied in computed tomography pulmonary angiography. The time that it takes for contrast to reach a predefined threshold in the pulmonary artery is called time to threshold (TTT). Our purpose was to analyse possible associations between TTT and circulatory state and prognosis in patients with acute pulmonary embolism (PE). In a single-centre, retrospective study 138 patients with PE and contrast administration via peripheral venous line were included. Clinical parameters of circulatory state were arterial pH, systolic blood pressure, heart rate, sPESI score, Wells score and GENEVA score. Survival was defined as surviving the following 30days after the PE diagnosis. Time to threshold was only weakly correlated with Fi02 (r=0.26, P=0.04), pH (r=-0.22, P=0.009), venous base excess (r=-0.18, P=0.04) and venous lactate (r=0.21, P=0.01). TTT did not correlate with clinical parameters/scores and mortality. There were weak associations between TTT and blood gas analysis parameters. There were no associations with clinically relevant prognosis scores and overall survival. Therefore, albeit TTT is an easily assessable parameter of CTPA, the potential use in clinical routine is limited for prognosis stratification in patients with PE.Therefore, albeit TTT is an easily assessable parameter of CTPA, the potential use in clinical routine is limited for prognosis stratification in patients with PE.This study was aimed at determining the roles and functions of lncRNA XIST/miR-545-3p/G3BP2 axis during hypoxia/reoxygenation (H/R)-induced H9C2 cell apoptosis. H9C2 cells were distributed into two groups, the H/R injury and control groups. High-throughput lncRNA sequencing was applied in the determination of differentially expressed lncRNAs between H/R-induced H9C2 cells and normal H9C2 cells. Real-time polymerase chain reactions (RT-PCR) were used to confirm the expression levels of lncRNA XIST in H/R-induced H9C2 cells. H9C2 cells were then transfected with lncRNA XIST recombinant plasmid (lncRNA XIST), sh-LINC XIST, agomiR-545-3p, antagomiR-545-3p, pcDNA-G3BP2, sh-G3BP2, and a corresponding negative control (NC). Bioinformatic analyses revealed that MiR-545-3p was a target for lncRNA XIST. This finding was confirmed by dual-luciferase reporter assay. The degree of cell apoptosis was evaluated by a flow cytometer. mTOR phosphorylation RT-PCR and western blot were performed to assess the apoptotic-related proteins in each group. A total of 859 differentially expressed lncRNAs (up-regulated = 502, down-regulated = 357) were identified. LncRNA XIST was found to be down-regulated in H/R-induced H9C2 cells while miR-545-3p was distinctly up-regulated. miR-545-3p was established to be a direct target for LncRNA XIST. LncRNA XIST significantly enhanced the apoptotic rate, while its inhibition suppressed the apoptotic rate. AgomiR-545-3p partially blocked the lncRNA XIST and enhanced the apoptosis of H/R-induced H9C2 cells. Moreover, miR-545-3p was shown to be a direct target for G3BP2. The overexpression of G3BP2 partially reversed the apoptotic effects of miR-545-3p on H/R-induced H9C2 cells. lncRNA XIST/miR-545-3p/GBP2 was found to be an apoptotic regulator in H/R-induced H9C2 cells.Epithelial-mesenchymal transition (EMT) has been contributed to increase migration and invasion of cancer cells. However, the correlate of Naa10p and IKKα with EMT in oral squamous cell carcinoma (OSCC) is not yet fully understood. In our present study, we found N-α-acetyltransferase 10 protein (Naa10p) and IκB kinase α (IKKα) were abnormally abundant in oral squamous cell carcinoma (OSCC). Bioinformatic results indicate that the expression of Naa10p and IKKα is correlated with TGF-β1/Smad and EMT-related molecules. The Transwell migration, invasion, qRT-PCR and Western blot assay indicated that Naa10p repressed OSCC cell migration, invasion and EMT, whereas IKKα promoted TGF-β1-mediated OSCC cell migration, invasion and EMT. Mechanistically, Naa10p inhibited IKKα activation of Smad3 through the interaction with IKKα directly in OSCC cells after TGF-β1 stimulation. Notably, knockdown of Naa10p reversed the IKKα-induced change in the migration, invasion and EMT-related molecules in OSCC cells after TGF-β1 stimulation.