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To describe the clinical presentation, diagnostic process, and surgical outcomes of late thoracic aortic stent graft infection (ASGI) with aerodigestive fistula. We retrospectively analyzed three late ASGI patients admitted between 2015 and 2025, supplemented by a narrative literature review. Case 1 presented with mediastinal abscess and aorto-esophageal fistula; Case 2 with aorto-esophageal and aorto-tracheal fistula; Case 3 with aorto-tracheoesophageal fistula. All three patients underwent surgical intervention: abscess debridement and drainage (Case 1); re-intervention with covered stent, esophageal resection, and lobectomy (Case 2); and staged aortic bypass (Case 3). The 30-day postoperative mortality rate was 1/3 (33.3%), and the 1-year mortality rate was 3/3 (100%). Late ASGI complicated by aerodigestive fistula carries an extremely poor prognosis. Early recognition and timely consideration of definitive source control may be important, but optimal management remains challenging.

Apoptosis of pulmonary microvascular endothelial cells (PMVECs) was considered to be closely related to the pathogenesis of acute lung injury (ALI). We aim to investigate whether IL-22 plays protective roles in lung injury through inhibiting the apoptosis of PMVECs. ALI model was induced through subcutaneous infusion of angiotensin II (Ang II). Lung injury and infiltration of inflammatory cells were evaluated by determining the PaO 2 /FiO 2 , calculation of dry to weight ratio in lung, and immunohistochemisty analysis. Apoptosis of PMVECs was determined using TUNEL assay and flow cytometry, respectively. Immunofluorescence and Western blot analysis were used to determine the expression and localization of STAT3, as well as the nucleus transmission of STAT3 from cytoplasm after IL22 treatment. Pathological findings showed ALI was induced 1 week after AngII infusion. IL22 inhibited the AngII-induced ALI, attenuated the edema in lung and the infiltration of inflammatory cells. Also, it contributed to the apoptosis of PMVECs induced by AngII. Meanwhile, significant increase was noticed in the expression of STAT3, phosphorylation of Y705-STAT3, and migration from cytoplasm to the nucleus after IL-22 treatment (P < 0.05). The activation of STAT3 by IL22 showed significant attenuation after AG490 treatment. Our data indicated that IL22 showed protective effects on lung injury through inhibiting the AngII-induced PMVECs apoptosis and PMVEC barrier injury by activating the JAK2/STAT3 signaling pathway.

Total arch replacement and stent trunk were performed for two patients. One of these underwent a total bilateral carotid artery replacement in anatomical position while the other underwent partial carotid artery dissection. The first patient demonstrated no neurological complication after surgery and a postoperative computed tomography angiography (CTA) showed bilateral common carotid artery patency. However, the second patient had neurological dysfunction after surgery, while a postoperative CTA showed occlusion of the left common carotid artery. Anatomical replacement for a common carotid artery dissection with thrombus has the potential to significantly improve cerebral perfusion and reduce postoperative neurological complications.

Angiotensin II (AngII) caused pulmonary microvascular endothelial barrier injury, which induced acute aortic dissection (AAD) combined with acute lung injury (ALI). However, the exact mechanism is unclear. We investigated the role of dephosphorylation of Y685-VE-cadherin in the AngII induced pulmonary microvascular endothelial barrier injury. Mice or pulmonary microvascular endothelial cells (PMVECs) were divided into control group, AngII group, AngII+PP2 (Src kinase inhibitor) group, and PP2 group. PP2 was used to inhibit the phosphorylation of Y685-VE-cadherin. Pathological changes, infiltration of macrophages and neutrophils, and pulmonary microvascular permeability were used to determine the pulmonary microvascular endothelial barrier function. Flow cytometry was used to determine the apoptosis of PMVECs, and immunofluorescence was used to determine the skeletal arrangement. Transendothelial resistance was used to detect the permeability of endothelial barrier. Phosphorylation of Y685-VE-cadherin was significantly reduced after AngII stimulation (P<0.05), together with skeletal rearrangement, and elevation of endothelial permeability which finally induced endothelial barrier injury. After PP2 interference, the phosphorylation of Y685-VE-cadherin was further reduced and the endothelial permeability was further elevated. These data indicated that AngII could induce pulmonary injury by triggering endothelial barrier injury, and such process may be related to the dephosphorylation of Y685-VE-cadherin and the endothelial skeletal rearrangement.

Abstract Total arch replacement and stent trunk were performed for two patients. One of these underwent a total bilateral carotid artery replacement in anatomical position while the other underwent partial carotid artery dissection. The first patient demonstrated no neurological complication after surgery and a postoperative computed tomography angiography (CTA) showed bilateral common carotid artery patency. However, the second patient had neurological dysfunction after surgery, while a postoperative CTA showed occlusion of the left common carotid artery. Anatomical replacement for a common carotid artery dissection with thrombus has the potential to significantly improve cerebral perfusion and reduce postoperative neurological complications.

The pathogenesis of acute aortic dissection (AAD) complicated acute lung injury (ALI) is not currently well defined. At present, no effective animal model has been established for AAD complicated ALI, which hinders research and development of an appropriate treatment regimen for the concurrent conditions. The aim of the present study was to evaluate the therapeutic effects of bindarit (Bnd), an indazolic derivative, on the production of monocyte chemoattractant protein (MCP)-1 in angiotensin II (AngII)-induced complicated ALI in rats. An AAD complicated ALI rat model was established using aminopropionitrile (BAPN) and AngII. The pathological features of AAD complicated ALI were assessed via biochemical and histopathological evaluations. AngII-stimulated human pulmonary microvascular endothelial cells (hPMVECs) were used to assess the effects of Bnd on MCP-1 expression. Western blot analysis was performed to analyze the expression of proteins that may be associated with the process. AAD complicated ALI was established following BAPN and AngII interference, and a massive accumulation of macrophages was observed in the lung tissues of the study rats. Bnd was able to significantly attenuate the incidence of AAD complicated ALI (P<0.05), and significantly inhibit the accumulation of macrophages (P<0.05). The overexpression of MCP-1 induced by AngII in hPMVECs was significantly inhibited by Bnd (P<0.05), which may be associated with downregulation of the classical nuclear factor-κB pathway. Bnd was able to attenuate the incidence of AAD complicated ALI, and inhibit the accumulation of macrophages in vivo. These findings provide a basis for future applications of Bnd as part of a therapeutic treatment schedule for aortic dissection complicated lung injury.

The pathogenesis of acute aortic dissection (AAD) complicated acute lung injury (ALI) is not currently well defined. At present, no effective animal model has been established for AAD complicated ALI, which hinders research and development of an appropriate treatment regimen for the concurrent conditions. The aim of the present study was to evaluate the therapeutic effects of bindarit (Bnd), an indazolic derivative, on the production of monocyte chemoattractant protein (MCP)-1 in angiotensin II (AngII)-induced complicated ALI in rats. An AAD complicated ALI rat model was established using aminopropionitrile (BAPN) and AngII. The pathological features of AAD complicated ALI were assessed via biochemical and histopathological evaluations. AngII-stimulated human pulmonary microvascular endothelial cells (hPMVECs) were used to assess the effects of Bnd on MCP-1 expression. Western blot analysis was performed to analyze the expression of proteins that may be associated with the process. AAD complicated ALI was established following BAPN and AngII interference, and a massive accumulation of macrophages was observed in the lung tissues of the study rats. Bnd was able to significantly attenuate the incidence of AAD complicated ALI (P<0.05), and significantly inhibit the accumulation of macrophages (P<0.05). The overexpression of MCP-1 induced by AngII in hPMVECs was significantly inhibited by Bnd (P<0.05), which may be associated with downregulation of the classical nuclear factor-KB pathway. Bnd was able to attenuate the incidence of AAD complicated ALI, and inhibit the accumulation of macrophages in vivo. These findings provide a basis for future applications of Bnd as part of a therapeutic treatment schedule for aortic dissection complicated lung injury. Key words: acute aortic dissection, lung injury, nuclear factor-KB pathway, bindarit

Circular RNAs (circRNAs) play important roles in miRNA function and transcriptional control. However, little is known regarding circRNAs in the pear. In this study, we identified circRNAs using deep sequencing and analyzed their expression under drought stress. We identified 899 circRNAs in total, among which 33 (23 upregulated, 10 downregulated) were shown to be dehydration-responsive. We performed GO and KEGG enrichment analysis to predict the functions of differentially expressed circRNAs. 309 circRNAs were predicted to act as sponges for 180 miRNAs. A circRNA-miRNA co-expression network was constructed based on correlation analysis between the differentially expressed circRNAs and their miRNA binding sites. Our study will provide a rich genetic resource for the discovery of genes related to drought stress, and can readily be applied to other fruit trees.

NSF’s ChemMatCARS, operated by the University of Chicago and located at the Advanced Photon Source (APS), continues to expand its capabilities in small molecule crystallography. NSF’s ChemMatCARS is undergoing an upgrade to enhance its cutting-edge diffractometers and detectors for advanced crystallographic techniques at 15-ID-B and 15-ID-D hutches. A new 15-ID-B hutch will support Diffraction Anomalous Fine Structure (DAFS) below 5 keV and features a new Mail-In service. 15-ID-D supports high-energy diffraction, in-situ diffraction, quantum crystallography and advanced structural dynamics. As part of this upgrade, we have commissioned Roadrunner, a high-precision diffractometer equipped with an on-axis camera and fast scanning capabilities. We’ve also deployed the first Pilatus 4 detector at APS, enabling fast, high- quality data collection. Additionally, we’ve developed a Field Programmable Gate Array (FPGA)-based Radio Frequency (RF) divider with fine phase delay for advanced timing experiments. These upgrades significantly enhance the program’s capabilities and accessibility for cutting-edge crystallographic research. This poster will provide an overview of the advanced crystallographic program at NSF’s ChemMatCARS, emphasizing the current capabilities and ongoing developments

The quality and life of the injected product are affected by surface quality of curved mold, and reasonable polishing method is the key to obtain the high-quality surface of curved mold. Small polishing tool is controlled by constant displacement polishing in the conventional method of robot polishing. The polishing force is adjusted to affect the surface quality of mold during mold polishing. The shortcomings of traditional control method of robot are investigated by simulation, and the constant force control approach is proposed to maintain stable force, which is achieved by a position-based impedance control algorithm. The polishing experiments of curved mold are conducted by using two control methods with constant displacement control polishing (CDCP) and constant force control polishing (CFCP), respectively. The experimental results show that the CFCP method can maintain polishing force stability and the reduction of surface roughness in the three groups of experiments using CDCP method is much lower than that of CFCP method, respectively. The feasibility of constant force control polishing method (CFCP) is verified.