Photocatalytic CO2 Reduction by Near-Infrared-Light (1200 nm) Irradiation and a Ruthenium-Intercalated NiAl-Layered Double Hydroxide.

Near-infrared light-driven photocatalytic CO2 reduction (NIR-CO2PR) holds tremendous promise for the production of valuable commodity chemicals and fuels. However, designing photocatalysts capable of reducing CO2 with low energy NIR photons remains challenging. Herein, a novel NIR-driven photocatalyst comprising an anionic Ru complex intercalated between NiAl-layered double hydroxide nanosheets (NiAl-Ru-LDH) is shown to deliver efficient CO2 photoreduction (0.887 µmol h-1) with CO selectivity of 84.81% under 1200 nm illumination and excellent stability over 50 testing cycles. This remarkable performance results from the intercalated Ru complex lowering the LDH band gap (0.98 eV) via a compression-related charge redistribution phenomenon. Furthermore, transient absorption spectroscopy data verified light-induced electron transfer from the Ru complex towards the LDH sheets, increasing the availability of electrons to drive CO2PR. The presence of hydroxyl defects in the LDH sheets promotes the adsorption of CO2 molecules and lowers the energy barriers for NIR-CO2PR to CO. To our knowledge, this is one of the first reports of NIR-CO2PR at wavelengths up to 1200 nm in LDH-based photocatalyst systems.

Comprehensive bioinformatics analysis revealed potential key genes and pathways underlying abdominal aortic aneurysm.

Abdominal aortic aneurysm (AAA) is a permanent, asymptomatic segmental dilatation of the abdominal aorta, with a high mortality risk upon rupture. Identification of potential key genes and pathways may help to develop curative drugs for AAA. We conducted RNA-seq on abdominal aortic tissues from both AAA patients and normal individuals as a control group. Integrated bioinformatic analysis was subsequently performed to comprehensively reveal potential key genes and pathways. A total of 1148 differential expressed genes (DEGs) (631 up-regulated and 517 down-regulated) were identified in our study. Gene Ontology (GO) analysis revealed enrichment in terms related to extracellular matrix organization, while KEGG analysis indicated enrichment in hematopoietic cell lineage and ECM-receptor interaction. Protein-protein interaction (PPI) network analysis revealed several candidate key genes, and differential expression of 6 key genes (CXCL8, CCL2, PTGS2, SELL, CCR7, and CXCL1) was validated by Gene Expression Omnibus (GEO) datasets. Receiver operating characteristic curve (ROC) analysis demonstrated these genes' high discriminatory ability between AAA and normal tissues. Immunohistochemistry indicated that several key genes were highly expressed in AAA tissues. Single-cell RNA sequencing revealed differential distribution patterns of these identified key genes among various cell types. 26 potential drugs linked to our key genes were found through DGIdb. Overall, our study provides a comprehensive evaluation of potential key genes and pathways in AAA, which could pave the way for the development of curative pharmacological therapies.

The Notch1/Hes1 signaling pathway affects autophagy by adjusting DNA methyltransferases expression in a valproic acid-induced autism spectrum disorder model.

As a pervasive neurodevelopmental disease, autism spectrum disorder (ASD) is caused by both hereditary and environmental elements. Research has demonstrated the functions of the Notch pathway and DNA methylation in the etiology of ASD. DNA methyltransferases DNMT3 and DNMT1 are responsible for methylation establishment and maintenance, respectively. In this study, we aimed to explore the association of DNA methyltransferases with the Notch pathway in ASD. Our results showed Notch1 and Hes1 were upregulated, while DNMT3A and DNMT3B were downregulated at the protein level in the prefrontal cortex (PFC), hippocampus (HC) and cerebellum (CB) of VPA-induced ASD rats compared with Control (Con) group. However, the protein levels of DNMT3A and DNMT3B were augmented after treatment with 3,5-difluorophenacetyl-L-alanyl-S-phenylglycine-2-butyl ester (DAPT), suggesting that abnormal Notch pathway activation may affect the expression of DNMT3A and DNMT3B. Besides, our previous findings revealed that the Notch pathway may participate in development of ASD by influencing autophagy. Therefore, we hypothesized the Notch pathway adjusts autophagy and contributes to ASD by affecting DNA methyltransferases. Our current results showed that after receiving the DNA methyltransferase inhibitor 5-Aza-2'-deoxycytidine (5-Aza-2'dc), the VPA + DAPT+5-Aza-2'dc (V + D + Aza) group exhibited reduced social interaction ability and increased stereotyped behaviors, and decreased expression of DNMT3A, DNMT3B and autophagy-related proteins, but did not show changes in Notch1 and Hes1 protein levels. Our results indicated that the Notch1/Hes1 pathway may adjust DNMT3A and DNMT3B expression and subsequently affect autophagy in the occurrence of ASD, providing new insight into the pathogenesis of ASD.

Intramolecular and Intermolecular Interaction Switching in the Aggregates of Perylene Diimide Trimer: Effect of Hydrophobicity.

The research on perylene diimide (PDI) aggregates effectively promotes their applications in organic photovoltaic solar cells and fluorescent sensors. In this paper, a PDI fabricated with three peripheral PDI units (N, N'-bis(6-undecyl) perylene-3,4,9,10-bis(dicarboximide)) is investigated. The trimer shows different absorption and fluorescence properties due to hydrophobicity when dissolved in the mixed solvent of tetrahydrofuran (THF) and water. Through comprehensive analysis of the fluorescence lifetime and transient absorption spectroscopic results, we concluded that the trimer underwent different excited state kinetic pathways with different concentrations of water in THF. When dissolved in pure THF solvent, both the intramolecular charge-transfer and excimer states are formed. When the water concentration increases from 0 to 50% (v/v), the formation time of the excimer state and its structural relaxation time are prolonged, illustrating the arising of the intermolecular excimer state. It is interesting to determine that the probability of the intramolecular charge-transfer pathway will first decrease and then increase as the speed of intermolecular excimer formation slows down. The two inflection points appear when the water concentration is above 10% and 40%. The results not only highlight the importance of hydrophobicity on the aggregate properties of PDI multimers but also guide the further design of PDI-based organic photovoltaic solar cells.

Safety and Efficacy of the Passeo-18 Lux Drug-Coated Balloon Catheter in Atherosclerotic Femoropopliteal Lesions: The Multicenter BIOLUX P-IV China Study.

BACKGROUND: The purpose of this trial was to assess the safety and effectiveness of a paclitaxel-coated balloon catheter in Chinese patients with de novo or nonstented restenotic femoropopliteal atherosclerotic lesions. METHODS: BIOLUX P-IV China is a prospective, independently adjudicated, multicenter, single-arm trial conducted in China. Patients with Rutherford class 2-4 were eligible, excluded were patients in which predilation resulted in severe (≥ grade D) flow-limiting dissection or residual stenosis > 70%. Follow-up assessments were conducted at 1, 6, and 12 months. The primary safety end point was 30-day major adverse event rate and the primary effectiveness end point was primary patency at 12 months. RESULTS: We enrolled 158 patients with 158 lesions. Mean age was 67.6 ± 9.6 years, diabetes was present in 53.8% (n = 85), and previous peripheral intervention/surgeries in 17.1% (n = 27). Lesions were 4.1 ± 0.9 mm in diameter and 74 ± 50 mm long with a mean diameter stenosis of 91 ± 13%; 58.2% (n = 92) were occluded (core laboratory analysis). Device success was achieved in all patients. The rate of major adverse events was 0.6% (95% confidence interval: 0.0; 3.5) at 30 days, consisting of 1 target lesion revascularization. At 12 months, binary restenosis was present in 18.7% (n = 26) and target lesion revascularization was performed in 1.4% (n = 2, all clinically driven), resulting in a primary patency of 80.0% (95% confidence interval: 72.4, 85.8); no major target limb amputation occurred. Clinical improvement at 12 months, defined as improvement of at least 1 Rutherford class, was 95.3% (n = 130). The median walking distance per 6-minute walk test was 279 m at baseline and improved by 50 m at 30 days and by 60 m at 12 months; the visual analogue scale changed from 76.6 ± 15.6 at baseline to 80.0 ± 15.0 at 30 days and 78.6 ± 14.6 at 12 months. CONCLUSIONS: Our results confirmed the clinical effectiveness and safety of a paclitaxel-coated peripheral balloon dilatation catheter for the treatment of de novo and nonstented restenotic lesion of the superficial femoral and proximal popliteal artery in Chinese patients (NCT02912715).

Comparison between endovascular aneurysm repair-selected and endovascular aneurysm repair-only strategies for the management of ruptured abdominal aortic aneurysms: An 11-year experience at a Chinese tertiary hospital.

Objectives: The aim of this study was to review our management experience of ruptured abdominal aortic aneurysms (RAAAs) using an endovascular aneurysm repair (EVAR)-only strategy, and discuss the feasibility of this strategy. Materials and methods: A retrospective analysis of clinical data was performed in patients with RAAAs from January 2009 to October 2020. Our strategy toward operative treatment for RAAAs evolved from an EVAR-selected (from January 2009 to April 2014) to an EVAR-only (from May 2014 to October 2020) strategy. Baseline characteristics, thirty-day mortality, perioperative complications, and long-term outcomes of patients were compared between the two periods. Results: A total of 93 patients undergoing emergent RAAA repair were eventually included. The overall operation rate in RAAAs at our centre was 70.5% (93/132). In the EVAR-only period, all 53 patients underwent ruptured endovascular aneurysm repair (rEVAR). However, only 47.5% (19/40) of patients in the EVAR-selected period underwent rEVAR, and the remaining 21 patients underwent emergent open surgery. Thirty-day mortality in the EVAR-only group was 22.6% (12/53) compared with 25.0% (10/40) for the EVAR-selected group (P = 0.79). Systolic blood pressure ≤70 mmHg [adjusted odds ratio (OR) 4.99, 95% confidence interval (CI), 1.13-22.08, P = 0.03] and abdominal compartment syndrome (adjusted OR 3.72, 95% CI, 1.12-12.32, P = 0.03) were identified as independent risk factors responsible for 30-day mortality. After 5 years, 47.5% (95% CI, 32.0-63.0%) of patients in the EVAR-selected group were still alive versus 49.1% (95% CI, 32.3-65.9%) of patients in the EVAR-only group (P = 0.29). Conclusion: The EVAR-only strategy has allowed rEVAR to be used in nearly all the RAAAs with similar mortality comparing with the EVAR-selected strategy. Due to the avoidance of operative modality selection, the EVAR-only strategy was associated with a more simplified algorithm, less influence on haemodynamics, and a shorter operation and recovery time.

Efficacy and safety of rivaroxaban in patients with inferior vena cava filter placement without anticoagulation contraindications (EPICT): a prospective randomised controlled trial study protocol.

INTRODUCTION: Inferior vena cava (IVC) filters are commonly used in patients with venous thromboembolism to prevent fatal pulmonary embolism, but the thrombosis risk increases after filter placement. Warfarin is a widely anticoagulant, but long-term monitoring and dose adjustments are required. Anticoagulation with rivaroxaban is more straightforward as it dose not require laboratory monitoring. This study compares the efficacy and safety of rivaroxaban and warfarin as an in anticoagulation therapy for patients with IVC filter placement. METHODS AND ANALYSIS: This is a multicentre, randomised controlled trial. In total, 200 patients with deep vein thrombosis (DVT) with IVC filter implantation from 10 hospitals will be recruited. The patients will be randomised to the experimental group (rivaroxaban) or the control group (nadroparin overlapped with warfarin). The primary outcomes include death of any cause, pulmonary embolism (PE)-related death, bleeding and recurrent PE/DVT. The secondary outcomes include the percentage of other vascular events, IVC filter retrieval failure and net clinical benefits. This study aims to provide reliable, verification for the efficacy and safety of rivaroxaban antithrombotic therapy after IVC filter placement. ETHICS AND DISSEMINATION: The study was approved by the Human Research Ethics Committee of the Second Affiliated Hospital of Zhejiang University School of Medicine (approval number: (2019) 295). The results will be disseminated through presentations at scientific conferences and publications in peer-reviewed journals TRIAL REGISTRATION NUMBER: NCT04066764.

Exosomal Transfer of miR-185 Is Controlled by hnRNPA2B1 and Impairs Re-endothelialization After Vascular Injury.

Dysfunction of endothelial cells (ECs) contributes to restenosis after vascular reconstruction for patients with coronary artery disease (CAD). The intercellular communication between ECs and vascular smooth muscle cells (VSMCs) might be critical in the development of restenosis and can be mediated by exosomes carrying functional microRNAs. miR-185 is reported to be associated with atherosclerosis, whether it plays a similar role in restenosis is unknown. In this study, we observed an elevated level of extracellular miR-185 in platelet-derived growth factor (PDGF)-stimulated VSMCs. The medium from PDGF-stimulated VSMCs promoted miR-185 expression in rat aortic ECs and inhibited EC angiogenesis. PDGF-stimulated VSMCs transferred miR-185 into ECs via exosomes. Furthermore, we found that the CXCL12 gene, a target of miR-185, is essential for the angiogenic potential of ECs. Exosomes derived from miR-185 mimic transfected VSMCs attenuated re-endothelialization after vascular injury. Moreover, we show that exosome-mediated miR-185 transfer is modulated by hnRNPA2B1. We also observed that hnRNPA2B1 is up-regulated during neointima formation and hnRNPA2B1 inhibition accelerates re-endothelialization and attenuates neointima formation following carotid injury. Taken together, our results indicate that exosomal miR-185 transfer from VSMCs to ECs is controlled by hnRNPA2B1 and impairs re-endothelialization after vascular injury.

Early-stage dynamics of chloride ion-pumping rhodopsin revealed by a femtosecond X-ray laser.

Chloride ion-pumping rhodopsin (ClR) in some marine bacteria utilizes light energy to actively transport Cl- into cells. How the ClR initiates the transport is elusive. Here, we show the dynamics of ion transport observed with time-resolved serial femtosecond (fs) crystallography using the Linac Coherent Light Source. X-ray pulses captured structural changes in ClR upon flash illumination with a 550 nm fs-pumping laser. High-resolution structures for five time points (dark to 100 ps after flashing) reveal complex and coordinated dynamics comprising retinal isomerization, water molecule rearrangement, and conformational changes of various residues. Combining data from time-resolved spectroscopy experiments and molecular dynamics simulations, this study reveals that the chloride ion close to the Schiff base undergoes a dissociation-diffusion process upon light-triggered retinal isomerization.

Long-term outcomes of endovascular treatment of isolated subclavian artery aneurysms.

OBJECTIVES: The aim of the present study was to review our institutional experience of endovascular treatment for isolated subclavian artery aneurysms and evaluate the long-term outcomes. METHODS: A retrospective review of all patients with isolated subclavian artery aneurysms who underwent endovascular treatment between March 2008 and March 2020 was performed. The demographics, aneurysmal characteristics, treatment strategies, and in-hospital and follow-up outcomes were recorded and then analyzed. RESULTS: From March 2008 to March 2020, 35 isolated subclavian artery aneurysms were endovascularly treated at our institution. Atherosclerosis was the most common cause of aneurysms in this series. Most aneurysms were intrathoracic (91.4%) and located at the right side (77.1%). There were 26 true aneurysms, seven pseudoaneurysms, and two ruptured isolated subclavian artery aneurysms. Five types of endovascular strategies were performed. Covered stent placement across the aneurysm was the most (54.3%) commonly used method. Technical success was achieved in all patients. The median postoperative in-hospital stay was 4.0 days (range, 1-15 days). One patient died after discharge but within 30 days of surgery due to myocardial infarction. The median follow-up time was 62.0 months (range, 3-132 months). No death, stroke, stent fractures, or severe upper limb ischemia developed during the follow-up period. The cumulative survival rate at five years was 97.1%. The overall complication rate was 25.7% and one-third of complications (8.6%) required reinterventions. CONCLUSIONS: Endovascular treatment for isolated subclavian artery aneurysms is safe, effective and technically achievable in most patients. Short- and long-term outcomes are promising. Reasonable and flexible use of covered stents can also get satisfactory outcomes in some complicated lesions such as isolated subclavian artery aneurysms located at the origin of the right subclavian artery, avoiding the huge surgical trauma caused by conventional open repair.

Coblation annuloplasty in cervical discogenic pain without radiculopathy.

INTRODUCTION: The nerve fibers innervating the annulus fibrosus are the major origin of degeneration-associated discogenic pain. Coblation is a tissue-dissociating technique in which the nerve fibers in the degenerative disc tissue are ablated. We hypothesized that coblation annuloplasty would be an effective maneuver for cervical discogenic pain without radiculopathy. AIM: To observe the therapeutic efficacy of coblation annuloplasty in patients with cervical discogenic pain without radiculopathy. MATERIAL AND METHODS: Forty patients diagnosed with cervical discogenic pain without radiculopathy were screened for coblation annuloplasty therapy. The patient-rated visual analog scale (VAS) score for pain, significant pain relief rate, and Modified MacNab pain-relieving effect were adopted to evaluate the therapeutic effect within a 1-year follow-up period. RESULTS: Thirty-three patients eventually completed the study. The average pain duration was 4.6 ±1.6 years (range: 0.5-8 years). The mean VAS pain score decreased from preoperative 6.8 ±0.9 to postoperative 2.5 ±1.3 (p < 0.01). For all participants, the immediate pain relief rate was 78.7% (26/33), which continued to postoperative 6 months. One year later, 22 (66.6%) subjects reported that their pain was significantly alleviated. According to the Modified MacNab criteria, 63.6-82.1% considered the effect of surgery for their pain therapy as "excellent" during the 1-year follow-up period. No significant complications such as hemorrhage, paresthesia, or infection were observed. CONCLUSIONS: This study is the first to demonstrate that coblation annuloplasty is an effective intervention providing significant alleviation of neck pain from cervical discogenic injury without radiculopathy.

CircCBFB-mediated miR-28-5p facilitates abdominal aortic aneurysm via LYPD3 and GRIA4.

HEADING AIMS: Abdominal aortic aneurysm (AAA) is featured by the growth impediment and apoptosis surge of VSMCs (vascular smooth muscle cells). MicroRNAs (miRNAs) are suggested to affect cellular behaviors including cell growth and apoptosis. This study concentrated on unraveling the emerging role of miR-28-5p in abdominal aortic aneurysm. MATERIALS AND METHODS: Previously, miR-28-5p was reported to be highly expressed in AAA. Functional assays were utilized to determine the role of miR-28-5p in VSMC apoptosis. To narrow down the downstream mRNAs, bioinformatics methods were utilized. The interaction between miR-28-5p and GRIA4 (glutamate ionotropic receptor AMPA type subunit 4) or LYPD3 (LY6/PLAUR domain containing 3) was explored. Candidate circRNAs (circular RNAs) of miR-28-5p were identified. Rescue analyses validated function of circCBFB (core-binding factor subunit beta)/miR-28-5p/GRIA4/LYPD3 axis in VSMC apoptosis and growth. KEY FINDINGS: MiR-28-5p acted as an apoptosis driver while circCBFB, GRIA4 and LYPD3 exerted anti-apoptosis effects in VSMCs. Mechanically, GRIA4 and LYPD3 were suppressed by miR-28-5p. Moreover, circCBFB served as a sponge of miR-28-5p, releasing GRIA4 and LYPD3 from miR-28-5p suppression. Functionally, GRIA4, LYPD3 and miR-28-5p were required in circCBFB-mediated VSMC apoptosis. SIGNIFICANCE: This work unveiled an innovative axis of circCBFB/miR-28-5p/GRIA4/LYPD3 in VSMC apoptosis, exerting its potential in providing new thoughts in AAA management.

A Modified Murine Abdominal Aortic Aneurysm Rupture Model Using Elastase Perfusion and Angiotensin II Infusion.

BACKGROUND: The perfused elastase AAA model and subcutaneous Angiotensin II infusion AAA model are widely used murine AAA models. We modified these two current models and developed a new murine model to study aneurysm formation and rupture. METHODS: The murine abdominal aorta was treated with elastase. Angiotensin II was infused at a dose of 1,000 ng/kg/min via an osmotic pump placed subcutaneously. A saline osmotic pump was used as the control. The aortas were harvested from the mice 4 weeks later, or earlier if mice died. The abdominal aorta was inspected using ultrasound and microscopy for aneurysm formation and/or signs of rupture. The aneurysm outcome was measured using aortic expansion and proinflammatory cytokine expression. It was also compared with the established conventional elastase perfusion and angiotensin II infusion abdominal aortic aneurysm models. RESULTS: By day 28 after surgery, all abdominal aortas of mice treated in the modified group had dilated and progressed to abdominal aortic aneurysms with 60% ruptured aneurysms, whereas none of the control aortas treated with saline became aneurysmal. In mice treated with elastase solution alone, 100% developed aneurysms and only one had a ruptured aneurysm. In mice given angiotensin II infusion alone, 37.5% developed aneurysms and none had a ruptured aneurysm. Histological examination of the modified murine abdominal aortic aneurysm rupture model was identical to that observed in the conventional elastase model. Quantitative polymerase chain reaction analysis revealed similarly increased levels of proinflammatory cytokines. CONCLUSIONS: We modified two current murine abdominal aortic aneurysm models to develop a murine abdominal aortic aneurysm model with consistent aneurysm formation and high rupture incidence, which can be used for studying abdominal aortic aneurysm rupture and treatment.

Chemical stabilization of the extracellular matrix attenuates growth of experimentally induced abdominal aorta aneurysms in a large animal model.

OBJECTIVE: The goal of the present study was to test the safety and efficacy of chemical stabilization of the arterial extracellular matrix as a novel nonoperative treatment of abdominal aortic aneurysms (AAAs) in a clinically relevant large animal model. METHODS: To achieve matrix stabilization, we used 1,2,3,4,6-pentagalloylglucose (PGG), a noncytotoxic polyphenolic agent capable of binding to and stabilizing elastin and collagen against the action of degrading enzymes. We first optimized the therapeutic PGG formulation and time of exposure by in vitro testing on porcine aortas using phenol histologic staining with iron chloride, elastic recoil assays, and PGG quantification as a function of tissue thickness. We then induced AAAs in 16 swine using sequential balloon angioplasty and elastase/collagenase and calcium chloride treatment of the infrarenal segment. We monitored AAA induction and development using digital subtraction angiography. At 2 weeks after induction, after the AAAs had reached ∼66% arterial expansion, the swine were randomly assigned to 2 groups. In the treatment group, we delivered PGG to the aneurysmal aorta endoluminally using a weeping balloon and evaluated the AAA diameters using digital subtraction angiography for another 10 weeks. The control swine did not receive any treatment. For the safety evaluation, we collected blood and performed comprehensive metabolic panels and complete blood counts every 2 to 3 weeks for all the animals. The swine were routinely monitored for neurologic and physical attributes such as behavior, inactivity, alertness, appetite, discomfort, and weight gain. After euthanasia and full necropsy, we analyzed the AAA tissue samples for PGG content, elastic recoil, and histologic features. RESULTS: In vitro, a single 2.5-minute intraluminal delivery of 0.3% PGG to the swine aorta was sufficient for PGG to diffuse through the entire thickness of the porcine arterial tissues and to bind with high affinity to the elastic lamellae, as seen by positive iron chloride staining, a reduction of elastic recoil, and an increase in PGG content. In vivo, the control swine AAA tissues were thickened and showed the typical aspects of AAA, including chronic inflammation, adventitial reactivity, smooth muscle cell proliferation, elastic lamellae degradation, and medial and adventitial calcification. Similar aspects were noted in the PGG-treated arteries, except for the lack of calcification and an apparent diminished hyperplasia. PGG treatment was effective in reducing AAA expansion and reversing the process of AAA dilation by reducing the aortic diameters to ≤30% by week 12 (P < .05). PGG was specifically localized to the aneurysmal segments as seen by histologic examination, the reduction of elastic recoil, and an increase in PGG content. PGG treatment did not affect the swine's neurologic or physical attributes, weight, blood chemistry, blood cells, or functionality of remote organs. The control, untreated swine exhibited progressive increases in AAA diameters up to a mean value of 104%. CONCLUSIONS: Localized delivery of PGG to the aneurysmal aorta attenuated AAA growth and reversed the course of the disease in the swine AAA model. Such specificity for diseased tissue is unprecedented in nonoperative AAA treatment. This novel paradigm-shifting approach has the potential to revolutionize AAA management and save thousands of lives.

Viabahn Open Revascularization Technique for Renal Artery Revascularization Reduces Renal Ischemia in Thoracoabdominal Aortic Aneurysm Hybrid Open-Endovascular Repair.

BACKGROUND: To improve hybrid open-endovascular repair, the Viabahn Open Revascularization Technique (VORTEC) has emerged as a sutureless method that reduces renal ischemia time. This study aimed to compare the differences between VORTEC and standard hybrid open-endovascular repair of thoracoabdominal aortic aneurysm (TAAA) in renal ischemia. METHODS: This is a retrospective analysis of 26 TAAA patients who underwent hybrid open-endovascular repair from April 2005 to April 2017. Twenty-one patients underwent standard hybrid open-endovascular repair, and 5 underwent VORTEC hybrid open-endovascular repair. RESULTS: Through April 2018, 26 patients were followed up for 48 ± 43 months. Nine patent renal arteries were revascularized by Viabahn in the VORTEC group, while 36 were revascularized with presewn multibranched grafts in the standard treatment group. The renal ischemia time was shorter in the VORTEC group than in the standard treatment group (5 ± 2 min vs. 15 ± 6 min). The increase in serum creatinine (SCr) on the first postoperative day in the standard treatment group was higher than that in the VORTEC group (1.68 ± 0.79 vs. 1.14 ± 0.05). Acute kidney injury (AKI) occurred in 5 patients in the standard treatment group (5/21, 24%). No patient experienced AKI in the VORTEC group (0/5, 0%). The renal artery (RA) patency rates in the VORTEC group were 100% (7/7) at both 1 week and 12 months after surgery. In the standard treatment group, the RA patency rates were 97% at 1 week (33/34) and 93% at 12 months (28/30) after surgery. CONCLUSIONS: VORTEC reduces renal ischemia time and decreases postoperative AKI in patients undergoing hybrid repair of thoracoabdominal aneurysms.

MicroRNA-187 Reduces Acute Ischemic Renal Podocyte Injury via Targeting Acetylcholinesterase.

BACKGROUND: Podocyte injury was reported to be involved in the major pathogenesis of ischemia/reperfusion (I/R)-induced ischemic acute renal failure. Our purpose was to study the mechanism of miR-187 improving I/R-induced podocytes injury. MATERIALS AND METHODS: The miR-187 mimics and inhibitor were transfected into the immortalized mouse podocyte (MPC-5) cells, and then transfected cells were subjected to hypoxia/reoxygenation (H/R, 3/3 h) to establish an H/R cell model. To investigate the effects of miR-187 on H/R-induced cell injury, cell viability and apoptosis were measured by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Dual-luciferase report system was used to verify whether miR-187 could directly target acetylcholinesterase (ACHE). The animal ischemia/reperfusion model was established and injected with miR-187 agomir. Kidney tissue sections were subjected to histological examination by hematoxylin and eosin staining to assess the renal injury. Real-time quantitative PCR and western blot were performed to determine gene expressions. RESULTS: The transfection of miR-187 mimics contributed to MPC-cells resistance to H/R-induced cell injury, which was reflected by enhanced cell viability and reduced apoptosis (from 20.05% to 9.43%) in H/R + negative control group. ACHE was confirmed as a target of miR-187, and ACHE siRNA had a similar efficiency to miR-187 mimic. The injection of miR-187 agomir not only effectively protected the kidney from I/R-induced injury, but also reduced the concentrations of serum creatinine. Moreover, nephrin was noticeably increased and desmin was decreased under the effects of agomir. CONCLUSIONS: Our findings indicated that miR-187 improved I/R-induced ischemic acute renal failure through protecting glomerular filtration barrier by blocking the expression of ACHE.

Uniform Alignment of Non-π-Conjugated Species Enhances Deep Ultraviolet Optical Nonlinearity.

The precision of array of laser applications and manipulation on smaller scales are limited by the so-called 200 nm wall, and breakthroughs rely on the discovery of new materials with transparency and phase matchability in the ultraviolet and deep ultraviolet region. Herein, we discover an unprecedented alignment of the asymmetric non-π-conjugated species [PO3F] in NaNH4PO3F·H2O, which allows the best uniform P-F bond orientation that generates a remarkable enhancement of the (010) in-plane anisotropy that yields the largest birefringence (obv.: 0.053) to date in the phosphate and fluorophosphate families. The substance produces second harmonic generation lasers through direct frequency doubling with incident Yb:KGW femtosecond lasers on an as-synthesized (010) wafer with a size of 14 × 10 × 2.1 mm3. According to the calculated refractive index dispersion curve, the shortest second-harmonic generation (SHG) wavelength is estimated to be 194 nm, the shortest among phosphates and monofluorophosphate. These insights may help to design other high-performance non-π-conjugated deep-UV nonlinear optical materials.

Exosomes from mesenchymal stem cells expressing miR-125b inhibit neointimal hyperplasia via myosin IE.

Intercellular communication between mesenchymal stem cells (MSCs) and their target cells in the perivascular environment is modulated by exosomes derived from MSCs. However, the potential role of exosome-mediated microRNA transfer in neointimal hyperplasia remains to be investigated. To evaluate the effects of MSC-derived exosomes (MSC-Exo) on neointimal hyperplasia, their effects upon vascular smooth muscle cell (VSMC) growth in vitro and neointimal hyperplasia in vivo were assessed in a model of balloon-induced vascular injury. Our results showed that MSC-Exo were internalised by VSMCs and inhibited proliferation and migration in vitro. Further analysis revealed that miR-125b was enriched in MSC-Exo, and repressed the expression of myosin 1E (Myo1e) by targeting its 3' untranslated region. Additionally, MSC-Exo and exosomally transferred miR-125b repressed Myo1e expression and suppressed VSMC proliferation and migration and neointimal hyperplasia in vivo. In summary, our findings revealed that MSC-Exo can transfer miR-125b to VSMCs and inhibit VSMC proliferation and migration in vitro and neointimal hyperplasia in vivo by repressing Myo1e, indicating that miR-125b may be a therapeutic target in the treatment of vascular diseases.

Application of triple-chimney technique using C-TAG and Viabahn or Excluder iliac extension in TEVAR treatment of aortic arch dilation diseases.

BACKGROUND: To report the experience of a single centre regarding the application of the triple-chimney technique using C-TAG with Viabahn or Excluder iliac extension devices for the endovascular management of aortic arch dilation diseases. METHODS: From July 2016 to August 2017, 7 patients (5 men; mean age 56.1±10.8 years) with aortic arch dilation diseases were treated with the triple-chimney technique. All patients were followed up at 1, 3, and 6 months and every 6 months thereafter. RESULTS: Six innominate arteries were deployed with Excluder iliac extensions and one with a Viabahn cover-stent. All the left common carotid arteries and left subclavian arteries were placed with Viabahn. Reverse chimney technique was applied in four patients. Three (42.0%) type I endoleaks were found on the final angiogram. Two were apparently reduced, and one disappeared after balloon dilation. The mean follow-up time was 15.7 months (9-20 months). All the type I endoleak was found disappeared within 3 months. One patient died of myocardial infarction at 6 months after discharge. No other complications such as stent-graft migration, occlusion, type II endoleak or neurological stroke occurred. CONCLUSIONS: The use of C-TAG coupled with Viabahn or Excluder iliac extension is feasible and effective for the treatment of aortic arch dilatation diseases. However, more patients and longer follow-up time are required to verify its long-term safety and efficacy.