Current status and future challenges in the endoscopic management of non-variceal upper gastrointestinal bleeding in children.

PURPOSE: This study aimed to elucidate the characteristics of non-variceal upper gastrointestinal bleeding (NVUGIB) in children and the outcomes of endoscopic hemostasis (EH) performed by pediatric surgeons. METHODS: We retrospectively reviewed the medical records of pediatric patients with NVUGIB who had undergone esophagogastroduodenoscopy (EGD) at our hospital, between December 2006 and March 2020. RESULTS: Thirty-six patients were included. The most common endoscopic diagnosis was gastritis (28%), followed by gastric ulcer (25%) and duodenal ulcer (25%). Thirty patients (83%) had underlying diseases, including a recent viral infection (39%), followed by Helicobacter pylori infection (14%). Fourteen patients (39%) underwent EH, exhibiting a high initial rate of hemostasis (100%). This was achieved in 12/14 patients by clipping. One patient was treated using a combination of a hypersaline and epinephrine (HSE) injection and coagulation therapy, as the ulcer exceeded the width of the hemoclips. Rebleeding occurred in one patient (7.1%) initially treated with pure ethanol injections. The partial view of the pediatric duodenum prevented the placement of hemoclips; hence, the patient was treated using a combination of HSE and coagulation therapy. CONCLUSION: Clipping, injection, and/or coagulation therapy can lead to high success rates for hemostasis, considering the anatomical characteristics in a pediatric population.

Analysis of nitroxyl spin probes in mouse brain by X-band ESR with microdialysis technique.

Stable nitroxyl radicals are widely used in electron spin resonance (ESR) studies in vivo to determine ROS generation, but there are insufficient data on how their distribution to various tissues, excretion, and/or systemic signal decay affect the signal decay in a region of interest. Here, we evaluated the level of spin probe in the brain using a microdialysis combined with X-band ESR spectroscopy, to clarify the BBB permeability of different spin probes. We also determined the association between PROXYL spin probe signal decay in the head and the probe's level in the brain, its excretion in urine, and its rate of signal decay in other areas and tissues. Dialysate recovered from the mouse prefrontal cortex was used to determine the total spin probe level in the brain by X-band ESR spectroscopy. There was a positive correlation between the level of spin probes in the brain and their partition coefficients. Furthermore, the in vivo decay rate of the nitroxyl radical signal in the head was associated with the probes' level in the brain, but not with its systemic signal decay rate or excretion into urine. These basic data may support the use of PROXYLs as site-specific ROS probes in the brain.

Modulation of the myocardial redox state by vagal nerve stimulation after experimental myocardial infarction.

AIMS: Redox alteration plays a major role in the pathogenesis of heart failure (HF). Since vagal nerve stimulation (VNS) is known to improve survival and attenuate cardiac remodelling, we hypothesized that VNS may modulate the myocardial redox state. METHODS AND RESULTS: Using a chronic HF mouse model, we applied VNS for 15 min and measured myocardial redox status using in vivo electron spin resonance spectroscopy. Signal decay rate of the nitroxyl probe, an index of redox status, was enhanced in HF compared with sham (0.16 +/- 0.01 vs. 0.13 +/- 0.01 min(-1), P < 0.05; n = 6), and VNS normalized this enhancement (0.13 +/- 0.01 min(-1), P < 0.05). Atropine sulphate abolished the VNS effects, indicating that the VNS modulates myocardial redox state via muscarinic receptors. N(omega)-Nitro-L-arginine methyl ester treatment and fixed-rate atrial pacing showed a trend to suppress the VNS effects, suggesting the involvement of nitric oxide-based signalling and myocardial oxygen consumption. Moreover, VNS decreased the myocardial norepinephrine (NE) level (0.25 +/- 0.07 vs. 0.60 +/- 0.12 ng/mL, P < 0.05; n = 6). Reactive oxygen species production from cultured cardiomyocytes was enhanced by beta-adrenergic activation, which was partially antagonized by 10 micromol/L acetylcholine (ACh) (relative value compared with control: NE 3.7 +/- 0.5, NE + ACh 2.5 +/- 0.3, P < 0.05; n = 12). CONCLUSION: The present study suggests that VNS modulates the cardiac redox status and adrenergic drive, and thereby suppresses free radical generation in the failing heart.

Fatty acids increase the circulating levels of oxidative stress factors in mice with diet-induced obesity via redox changes of albumin.

Plasma concentrations of free fatty acids are increased in metabolic syndrome, and the increased fatty acids may cause cellular damage via the induction of oxidative stress. The present study was designed to determine whether the increase in fatty acids can modify the free sulfhydryl group in position 34 of albumin (Cys34) and enhance the redox-cycling activity of the copper-albumin complex in high-fat diet-induced obese mice. The mice were fed with commercial normal diet or high-fat diet and water ad libitum for 3 months. The high-fat diet-fed mice developed obesity, hyperlipemia, and hyperglycemia. The plasma fatty acid/albumin ratio also significantly increased in high-fat diet-fed mice. The increased fatty acid/albumin ratio was associated with conformational changes in albumin and the oxidation of sulfhydryl groups. Moreover, an ascorbic acid radical, an index of redox-cycling activity of the copper-albumin complex, was detected only in the plasma from obese mice, whereas the plasma concentrations of ascorbic acid were not altered. Plasma thiobarbituric acid reactive substances were significantly increased in the high-fat diet group. These results indicate that the increased plasma fatty acids in the high-fat diet group resulted in the activated redox cycling of the copper-albumin complex and excessive lipid peroxidation.