Perioperative arterial cannulation in children is routinely performed. Based on clinical observation of several complications related to femoral arterial lines, the authors performed a larger study to further examine complications. The authors aimed to (1) describe the use patterns and incidence of major short-term complications associated with arterial cannulation for perioperative monitoring in children, and (2) describe the rates of major complications by anatomical site and age category of the patient. The authors examined a retrospective cohort of pediatric patients (age less than 18 yr) undergoing surgical procedures at a single academic medical center from January 1, 2006 to August 15, 2016. Institutional databases containing anesthetic care, arterial cannulation, and postoperative complications information were queried to identify vascular, neurologic, and infectious short term complications within 30 days of arterial cannulation. There were 5,142 arterial cannulations performed in 4,178 patients. The most common sites for arterial cannulation were the radial (N = 3,395 [66.0%]) and femoral arteries (N = 1,528 [29.7%]). There were 11 major complications 8 vascular and 3 infections (overall incidence, 0.2%; rate, 2 per 1,000 lines; 95% CI, 1 to 4) and all of these complications were associated with femoral arterial lines in children younger than 5 yr old (0.7%; rate, 7 per 1,000 lines; 95% CI, 4 to 13). The majority of femoral lines were placed for cardiac procedures (91%). Infants and neonates had the greatest complication rates (16 and 11 per 1,000 lines, respectively; 95% CI, 7 to 34 and 3 to 39, respectively). The overall major complication rate of arterial cannulation for monitoring purposes in children is low (0.2%). All complications occurred in femoral arterial lines in children younger than 5 yr of age, with the greatest complication rates in infants and neonates. There were no complications in distal arterial cannulation sites, including more than 3,000 radial cannulations. Observational studies highlight associations of C-reactive protein (CRP), a general marker of inflammation, and interleukin 6 (IL-6), a cytokine-stimulating CRP production, with individual depressive symptoms. However, it is unclear whether inflammatory activity is associated with individual depressive symptoms and to what extent metabolic dysregulation underlies the reported associations. To explore the genetic overlap and associations between inflammatory activity, metabolic dysregulation, and individual depressive symptoms. Genome-wide association study (GWAS) summary data of European individuals, including the following CRP levels (204 402 individuals); 9 individual depressive symptoms (3 of which did not differentiate between underlying diametrically opposite symptoms [eg, insomnia and hypersomnia]) as measured with the Patient Health Questionnaire 9 (up to 117 907 individuals); summary statistics for major depression, including and excluding UK Biobank participants, resulting in sample sizes of 50RP levels and individual depressive symptoms, which may result from the potentially causal association of metabolic dysregulation with anhedonia, tiredness, changes in appetite, and feelings of inadequacy. The study also found that IL-6 signaling is associated with suicidality. These findings may have clinical implications, highlighting the potential of anti-inflammatory approaches, especially IL-6 blockade, as a putative strategy for suicide prevention.Recent investigations have shown that multiple d-amino acids are present in mammals and these compounds have distinctive physiological functions. Free d-glutamate is present in various mammalian tissues and cells and in particular, it is presumably correlated with cardiac function, and much interest is growing in its unique metabolic pathways. Recently, we first identified d-glutamate cyclase as its degradative enzyme in mammals, whereas its biosynthetic pathway in mammals is unclear. Glutamate racemase is a most probable candidate, which catalyzes interconversion between d-glutamate and l-glutamate. Here, we identified the cDNA encoding l-serine dehydratase-like (SDHL) as the first mammalian clone with glutamate racemase activity. This rat SDHL had been deposited in mammalian databases as a protein of unknown function and its amino acid sequence shares ∼60% identity with that of l-serine dehydratase. Rat SDHL was expressed in Escherichia coli, and the enzymatic properties of the recombinant were characterized. The results indicated that rat SDHL is a multifunctional enzyme with glutamate racemase activity in addition to l-serine/l-threonine dehydratase activity. This clone is hence abbreviated as STDHgr. Further experiments using cultured mammalian cells confirmed that d-glutamate was synthesized and l-serine and l-threonine were decomposed. It was also found that SDHL (STDHgr) contributes to the homeostasis of several other amino acids.The Na+-coupled citrate transporter (NaCT/SLC13A5/mINDY) in the liver delivers citrate from the blood into hepatocytes. As citrate is a key metabolite and regulator of multiple biochemical pathways, deletion of Slc13a5 in mice protects against diet-induced obesity, diabetes, and metabolic syndrome. Silencing the transporter suppresses hepatocellular carcinoma. Therefore, selective blockers of NaCT hold the potential to treat various diseases. Here we report on the characteristics of one such inhibitor, BI01383298. It is known that BI01383298 is a high-affinity inhibitor selective for human NaCT with no effect on mouse NaCT. Here we show that this compound is an irreversible and non-competitive inhibitor of human NaCT, thus describing the first irreversible inhibitor for this transporter. The mouse NaCT is not affected by this compound. The inhibition of human NaCT by BI01383298 is evident for the constitutively expressed transporter in HepG2 cells and for the ectopically expressed human NaCT in HEK293 cells. The IC50 is ∼100 nM, representing the highest potency among the NaCT inhibitors known to date. Exposure of HepG2 cells to this inhibitor results in decreased cell proliferation. We performed molecular modeling of the 3D-structures of human and mouse NaCTs using the crystal structure of a humanized variant of VcINDY as the template, and docking studies to identify the amino acid residues involved in the binding of citrate and BI01383298. Cevidoplenib purchase These studies provide insight into the probable bases for the differential effects of the inhibitor on human NaCT versus mouse NaCT as well as for the marked species-specific difference in citrate affinity.