Evaluation of the input site and characteristics of the antegrade fast pathway based on three-dimensional bi-atrial stimulus-ventricle mapping

Journal of Interventional Cardiac Electrophysiology - Previous studies examined the right atrial (RA) input site of the antegrade fast pathway (AFp) (AFpI). However, the left atrial (LA) input to...     

Facile determination of natural cannabinoids in cannabis products using a conventional fully porous particle column and isocratic high-performance liquid chromatography with diode-array detector

Forensic Toxicology -     

Interleukin-17A promotes rheumatoid arthritis synoviocytes migration and invasion under hypoxia by increasing MMP2 and MMP9 expression through NF-κB/HIF-1α pathway

Both hypoxia and interleukin-17A (IL-17A) promote the migration and invasion of fibroblast-like synoviocytes (FLSs), which are critical for the pathogenesis of rheumatoid arthritis (RA). However, the biochemical pathways regulating IL-17A combined with hypoxia are not well defined. In this study, we found that co-stimulating RA-FLSs with IL-17A and hypoxia did not appear to promote the epithelial–mesenchymal transition (EMT), but did increase cell motility. We further showed that a proinvasive effect of IL-17A on FLSs under hypoxia might be through upregulation of matrix metalloproteinase 2 (MMP2) and MMP9. Moreover, IL-17A-induced expression of MMP2 and MMP9 under hypoxia was accompanied by increased activation of nuclear factor-κB (NF-κB)/hypoxia-inducible factor-1α (HIF-1α). Knockdown or inhibition of HIF-1α and NF-κB by small interfering RNA or specific small molecule inhibitors blocked IL-17A-mediated and hypoxia-mediated MMP2 and MMP9 expression, cell migration, and invasion. In addition, the inhibition of NF-κB led to a marked decrease in the expression of HIF-1α, which indicated that IL-17A activated HIF-1α via the NF-κB pathway in hypoxia. Taken together, our observations suggest a synergetic effect of IL-17A and hypoxia that might contribute to the migration and invasion of RA-FLSs by upregulating the expression of MMP2 and MMP9 by activation of the NF-κB/HIF-1α pathway.     

Effects of electrical microstimulation of peripheral sympathetic nervous fascicle on glucose uptake in rats

Artificial pancreas systems control insulin-mediated glucose uptake. Although these systems are widely used in the clinical setting, they are still fraught with structural and biological problems. The non-insulin mediated glucose uptake (NIMGU) mechanism could be an alternative candidate as a target system for the artificial control of peripheral glucose uptake. Although the sympathetic nervous system is known to be one of the regulators of NIMGU, the effects of peripheral sympathetic activation on glucose uptake have not been well documented. We electrically stimulated a sympathetic nerve fascicle to clarify the possibility of controlling peripheral glucose uptake. A sympathetic signal was microneurographically obtained in the unilateral sciatic nerve in normal (NRML), insulin-resistant high-fat-fed (HFF), and streptozotocin-induced insulin-depleted (STZ) rats, and electrical stimulation was applied via the microelectrode (microstimulation). The microstimulation was also applied to sites other than the sympathetic fascicles in an additional group of normal rats (NSYMP group). The stimulation applied to the sympathetic fibers resulted in an immediate and transient decrease of blood glucose (BG) in the NRML, HFF, and STZ groups, with little change in the plasma insulin. The change in BG level seemed to depend on the basal BG level (NRML < HFF < STZ). In contrast, no reduction in BG was observed in the NSYMP group. These results suggest that microstimulation in the peripheral sympathetic fascicle could enhance glucose uptake in peripheral tissues—independently of insulin function—and show an alternative possibility for controlling glucose uptake.     

Long-term trend in serum (1,3)-β-D-glucan level in a man with chronic disseminated candidiasis treated with corticosteroids

Chronic disseminated candidiasis (CDC) is a type of invasive candidiasis. CDC commonly appears in the neutrophil recovery phase after chemotherapy in patients with hematologic malignancies, and immune reconstitution inflammatory syndrome (IRIS) is thought to play a major role in CDC development. This report describes the case of a 33-year-old man with CDC as a complication of acute myeloid leukemia. We describe the clinical course, body temperature, therapy, and (1,3)-β-D-glucan (BDG) levels over the course of 22 months. He was initially treated with antifungals, but corticosteroids were added because of a persistently elevated body temperature, which we attributed to IRIS. After starting corticosteroids, his clinical condition improved, but his BDG levels became markedly elevated. We hypothesize that the suppression of the excessive immune response by corticosteroids lead to granuloma collapse, fungal release, and hematogenous dissemination, resulting in elevated BDG levels. The patient's condition gradually improved over the course of follow-up.