Case Report: Successful Use of Biliary Stent for Iatrogenic Esophageal Perforation Following Balloon Dilation in a 7-Month-Old Infant.

Esophageal perforation is a rare but critical emergency that requires early detection and prompt management. In the pediatric population, iatrogenic injury is the most common etiology of esophageal perforation, and the majority of cases come from stricture dilation. Treatment options include medical management, endoscopic therapy, and surgery. Usually, conservative treatment is appropriate in most carefully selected patients, especially in the setting of early diagnosis and with the absence of severe sepsis. A surgical approach is reserved for a large tear with mediastinum contamination, or clinical deterioration after unsuccessful conservative management. With the advancement of the endoscopy technique, endoscopy therapy using esophageal stents is an available choice for adult populations who have a complicated protracted healing course or comorbidities precluding surgical attempts. However, this procedure is seldom implemented in children, especially in young infants, owing to unavailable equipment and experts. We report our successful use of a fully-covered self-expandable metal biliary stent in managing esophageal perforation in a seven-month-old infant. In light of this encouraging achievement, this model can be applied to more children who have the same problem.

Cyclophilin A is associated with peripheral artery disease and chronic kidney disease in geriatrics: The Tianliao Old People (TOP) study.

Cyclophilin A (CyPA), secreted by vascular smooth muscle cells in response to oxidative stress, is important in the pathogenesis of progressive peripheral arterial occlusion disease (PAOD), which is common among chronic kidney disease. We explored the prevalence of PAOD in Taiwan's elderly (≥ 65 years old) population and its association with CyPA and renal function. Residents of Tianliao District, a rural community in southern Taiwan, were surveyed. An ankle-brachial index (ABI) < 0.91 was defined as PAOD. Chronic kidney disease (CKD) was defined based on eGFR levels < 60 mL/min/1.73 m(2). Serum CyPA was measured. Of the 473 participants, 68 (14.4%) had PAOD. Multiple logistic regression analysis showed PAOD was significantly associated with lower eGFR, lower BMI, higher glycated hemoglobin and higher pulse pressure. Serum CyPA levels in participants with PAOD were significantly higher than those with normal ABI values (47.3 ± 0.4 vs. 25.5 ± 0.2 ng/mL, p < 0.001). Moreover, eGFR inversely correlated with serum CyPA level (p < 0.05) in participants with CKD, but not in participants with normal renal function. In conclusion, with a prevalence of PAOD as high as 14.4% in an elderly community, CyPA might be the link between PAOD and advanced impaired renal function.

Versatile regulation of cytosolic Ca2+ by vanilloid receptor I in rat dorsal root ganglion neurons.

Analysis of small dorsal root ganglion (DRG) neurons revealed novel functions for vanilloid receptor 1 (VR1) in the regulation of cytosolic Ca(2+). The VR1 agonist capsaicin induced Ca(2+) mobilization from intracellular stores in the absence of extracellular Ca(2+), and this release was inhibited by the VR1 antagonist capsazepine but was unaffected by the phospholipase C inhibitor xestospongins, indicating that Ca(2+) mobilization was dependent on capsaicin receptor binding and was not due to intracellular inositol-1,4,5-trisphosphate generation. Confocal microscopy revealed extensive expression of VR1 on endoplasmic reticulum, consistent with VR1 operating as a Ca(2+) release receptor. The main part of the capsaicin-releasable Ca(2+) store was insensitive to thapsigargin, a selective endoplasmic reticulum Ca(2+)-ATPase inhibitor, suggesting that VR1 might be predominantly localized to a thapsigargin-insensitive endoplasmic reticulum Ca(2+) store. In addition, VR1 was observed to behave as a store-operated Ca(2+) influx channel. In DRG neurons, capsazepine attenuated Ca(2+) influx following thapsigargin-induced Ca(2+) store depletion and inhibited thapsigargin-induced inward currents. Conversely, transfected HEK-293 cells expressing VR1 showed enhanced Ca(2+) influx and inward currents following Ca(2+) store depletion. Combined data support topographical and functional diversity for VR1 in the regulation of cytosolic Ca(2+) with the plasma membrane-associated form behaving as a store-operated Ca(2+) influx channel and endoplasmic reticulum-associated VR1 possibly functioning as a Ca(2+) release receptor in sensory neurons.