Extracellular vesicle-mediated transfer of lncRNA CLDN10-AS1 aggravates low-density lipoprotein-induced vascular endothelial injury.

Oxidized low-density lipoprotein (ox-LDL) stimulation impairs the oxidation-reduction equilibrium in vascular endothelial cells (VECs) and contributes to atherosclerosis (AS). This study probed the mechanisms of extracellular vesicle (EV)-mediated transfer of lncRNA CLDN10 antisense RNA 1 (CLDN10-AS1) in ox-LDL-induced VEC injury. Initially, VEC injury models were established by treating human umbilical vein endothelial cells (HUVECs) with ox-LDL. EVs were isolated from HUVECs (HUVECs-EVs) and identified. CLDN10-AS1, microRNA (miR)-186, and Yin Yang 1 (YY1) expressions in ox-LDL-treated HUVECs and EVs derived from these cells (ox-EVs) were measured. HUVECs were incubated with EVs, after which the cell viability, apoptosis, and concentrations of proinflammatory cytokines and oxidative stress markers were measured. We discovered that CLDN10-AS1 and YY1 were upregulated in ox-LDL-treated HUVECs, whereas miR-186 was downregulated. ox-EVs treatment elevated CLDN10-AS1 expression in HUVECs and ox-EVs overexpressing CLDN10-AS1 promoted VEC injury. Besides, CLDN10-AS1 is competitively bound to miR-186 and promoted YY1 expression. Rescue experiments revealed that miR-186 overexpression or YY1 suppression partially reversed the roles of ox-EVs overexpressing CLDN10-AS1 in ox-LDL-induced VEC injury. Lastly, clinical serum samples were collected for verification. Overall, CLDN10-AS1 carried by HUVECs-EVs into HUVECs competitively bound to miR-186 to elevate YY1 expression, thereby aggravating ox-LDL-induced VEC injury.

Mechanism and Management of Retrograde Type A Aortic Dissection Complicating TEVAR for Type B Aortic Dissection.

BACKGROUND: This study is to investigate the causes, treatment methods, and preventive measures of retrograde type A aortic dissection (RAAD) complicating thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD). METHODS: From January 2005 to December 2013, 360 TBAD patients receiving TEVAR were enrolled in this study. Among them, 304 cases were male and 56 cases were female. They were from 19 to 85 years old, with a mean age of 52 ± 12.8 years old. The average follow-up time was 32 ± 11.3 months (3-63 months), the follow-up rate was 69.1% (249 cases), and the lost rate was 30.9% (111 cases). The reasons and the treatment methods of RAAD complicating TEVAR for TBAD were analyzed. RESULTS: There were 5 cases of RAAD complicating TEVAR in TBAD (1.4%) patients, among them, 4 cases were male and 1 case was female. TEVAR operation failed in 1 case because of RAAD occurrence during TEVAR. This case was treated with open operation. In the other 4 cases, TEVAR operation was successfully carried out. During follow-up, RAAD was found in 3 cases within 1 month after TEVAR and in 1 case at 1 year after TEVAR. Conservative treatment was applied to 2 cases, whereas surgical operation treatment was performed in the other 3 cases. One case of conservative treatment patient was dead, and the other 4 cases are still alive. CONCLUSIONS: Incomplete design of stent-graft system, rough handling and presence of vascular wall lesions are the main reasons of RAAD complicating TEVAR for TBAD. Surgical operation is the most effective treatment measure for RAAD complicating TEVAR for TBAD.

Study on the small intestine absorptive kinetics characters of tanshinol and protocatechualdehyde of Salvia miltiorrhiza extracts in rats in vivo.

In order to provide scientific basis for clinical selection of drugs, to compare and analyze the effective constitutes and the intestinal absorption in vivo in rats of the compound salvia tablets and compound salvia dropping pills (taken as the representatives). Determine the contents of tanshinol, protocatechuic aldehyde, salvianolic acid B and tanshinone II A, cryptotanshinone, ginseng saponin Rg1 and Rb1 in the compound salvia tablets and compound salvia dropping pills by High Performance Liquid Chromatography (HPLC). The intestinal absorption condition of the tanshinol, protocatechuic aldehyde, salvianolic acid B of the compound salvia tablets and compound salvia dropping pills in rats were detected by intestinal perfusion experiment. Only the intake of protocatechuic aldehyde in the compound salvia tablets was higher than in the compound dropping pills, the intake of the other 6 effective constitutes were all lower than in the compound dropping pills. The intestinal absorption of protocatechuic aldehyde was rather complete, while the intestinal absorption of tanshinol and salvianolic acid B were not significant. The duodenum was the main absorption region of these three components. The absorption of protocatechuic aldehyde was different in different regions of the intestines. Each intake of the effective constitutes in the tablets and dropping pills were significantly different, and the rat intestinal absorption of part of the components were different.

Ultrasensitive colorimetric carcinoembryonic antigen biosensor based on hyperbranched rolling circle amplification.

In this study, a hyperbranched rolling circle amplification (HRCA)-based colorimetric biosensor for carcinoembryonic antigen (CEA) is developed with high sensitivity and specificity. A CEA aptamer can bind with its target (CEA) to form a complex due to their high affinity, and the introduced CDNA cannot hybridize with the aptamer. Thus, free CDNA can propagate the HRCA reaction to form a large number of single-stranded DNA (ss-DNA). ss-DNA can be easily adsorbed onto AuNPs and prevent salt-induced AuNPs aggregation, which causes the change in the color of the system. It is found that the absorbance intensity ratio (A520/A660) has a linear relationship with the concentration of the target in the range of 5 pM-0.5 nM, and the detection limit is as low as 2 pM (S/N = 3).

[Promoting effects and mechanisms of prostaglandin E1 on proliferation and migration of endothelial cells].

OBJECTIVE: To investigate the mechanism(s) that prostaglandin E1 (PGE1) promotes human umbilical vein endothelial cell (HUVEC)proliferation and migration. METHODS: Western blot, enzyme linked immunosorbent assay, cell proliferation and cell migration tests, and tube formation were used for analyzing the roles and mechanisms of PGE1 on HUVEC; Western blot was used for analyzing the effects of PGE1 on the expression of vascular endothelial growth factor (VEGF) in rat aortic vascular smooth muscle cells (VSMC). RESULTS: PGE1 significantly increased VEGF expression of HUVEC in time and a dose dependent manner with concomitantly increased HUVEC proliferation; treatment of HUVEC with Bevacizumab apparently suppressed PGE1-stimulated VEGF expression, which led to decreased tube formation, reduced cell proliferation and migration by 41% and 38%, respectively, compared with PGE1 treatment alone; PGE1 time-dependently induced both phosphorylation of ERK and p38 in HUVEC, whereas ERK inhibitor, PD98059, or p38 inhibitor, SB203580, blocked PGE1-induced VEGF expression of HUVEC, resulting in dramatically suppression of HUVEC proliferation and migration compared with PGE1 treatment alone (60% and 55% by PD98059, 62% and 51% by SB203580, respectively); in addition, cAMP-dependent protein kinase A inhibitor, H89 or Rp-cAMP blocked PGE1-induced VEGF expression in VSMC. CONCLUSION: PGE1 promotion of proliferation, migration and tube formation of HUVEC via VEGF further provides a novel theoretical support in efficacy of PGE1 treatment of critical limb ischemia and other related diseases.

Endovascular repair for abdominal aortic aneurysms involving visceral arteries: Effectiveness and contributing factors.

Objective: Abdominal aortic aneurysms (AAA) involving branches of the visceral arteries mainly refer to AAA with flat renal artery (neck length ≤5 mm) or beyond the renal artery, and the branch of the visceral arteries needs to be reconstructed during treatment. Endoluminal repair (EVR) surgery refers to the isolation of AAA with less surgical trauma through vascular puncture, guidewire, catheter, stent and double suturer technology. However, postoperative endoleak is a complication specific to open surgery. This study aimed to analyze the efficacy of EVR for AAA involving visceral vessels (AAA-Vs) and the factors influencing the occurrence of postoperative endoleak. Methods: A total of 106 patients with AAA-Vs in our hospital during the period of January 2018 to January 2022 were distinguished as the observation group (received EVR, n = 48) and the control group (received laparotomy, n = 58). The operation time, intraoperative bleeding, intraoperative blood transfusion, postoperative intensive care unit (ICU) observation time, postoperative food-taking time, first time out of bed, hospital stay, complications and the one-year mortality of two groups were compared. According to the occurrence of postoperative endoleak, the patients underwent endoluminal repair surgery were graded as non-endoleak group (n = 39) and endoleak group (n = 9). The clinical data, including aneurysm anatomical conditions (proximal neck length, neck diameter, proximal neck angle), tumor shape (normal, calcification, mural thrombus), and internal iliac artery embolism of two groups were compared. Logistic regression analysis was employed to analyze the risk factors of endoleak after EVR of AAA. Results: The operation time, intraoperative blood loss, intraoperative blood transfusion, postoperative ICU observation time, postoperative food-taking time, first time out of bed and hospitalization days were sharply lower in the observation group than the control group (P < 0.001). There existed no significant difference in the proportion of pulmonary complications, cardiac complications and electrolyte disorders between two groups (P > 0.05). The observation group had much lower incidence of incision infection complications than the control group (P < 0.05). The one-year mortality rate in the observation group was 10.42 %, markedly lower than 25.86 % in the control group (P < 0.05). The incidence of endoleak in the observation group was 18.75 %, while no internal endoleak occurred in the control group (P < 0.05). The proportion of male patients, smoking history, internal iliac artery embolism, and the level of tumor neck length and proximal tumor neck angle in the endoleak group were memorably higher in comparison with the non-endoleak group (P < 0.05). Logistic regression analysis revealed that the length of the neck and the angle of the proximal neck were independent risk factors for postoperative endoleak of AAA (P < 0.05). In conclusion: EVR was effective for AAA-Vs with the advantages of small trauma, rapid recovery, low complication rate and high safety. The diameter of the aneurysm neck and the angle of the proximal aneurysm neck were the risk factors for the occurrence of endoleak after EVR. It was necessary to fully evaluate the aneurysm before operation to help reduce the incidence of endoleak.

Engineering strategies and optimized delivery of exosomes for theranostic application in nerve tissue.

Severe injuries or diseases affecting the peripheral and central nervous systems can result in impaired organ function and permanent paralysis. Conventional interventions, such as drug administration and cell-based therapy, exhibit limited effectiveness due to their inability to preserve post-implantation cell survival and impede the deterioration of adjacent tissues. Exosomes have recently emerged as powerful tools for tissue repair owing to their proteins and nucleic acids, as well as their unique phospholipid properties, which facilitate targeted delivery to recipient cells. Engineering exosomes, obtained by manipulating the parental cells or directly functionalizing exosomes, play critical roles in enhancing regenerative repair, reducing inflammation, and maintaining physiological homeostasis. Furthermore, exosomes have been shown to restore neurological function when used in combination with biomaterials. This paper primarily focuses on the engineering strategies and delivery routes of exosomes related to neural research and emphasizes the theranostic application of optimized exosomes in peripheral nerve, traumatic spinal cord, and brain injuries. Finally, the prospects of exosomes development and their combination with other approaches will be discussed to enhance our knowledge on their theranostic effectiveness in neurological diseases.

Ameliorative Effects of Extracellular Vesicles Derived from Mesenchymal Stem Cells on Apoptosis and Differentiation of Osteoblasts Treated with CoCl2.

Severe osteoporotic fracture occurring in sites with inadequate blood supply can cause irreversible damage to cells, particularly osteoblasts, with current drug and surgical interventions exhibiting limitations for elderly individuals. As participants mediating intercellular communication, extracellular vesicles (EVs) are rarely reported to play functional roles in osteoblasts under hypoxia. Our study mainly investigated the effects of bone marrow mesenchymal stem cells-derived EVs (BMSCs-EVs) on apoptosis and differentiation of osteoblasts treated with CoCl2. Primary rat BMSCs and osteoblasts were extracted as required for the following experiments. Cell counting kit 8 assay was used to explore the concentration of CoCl2 for treating osteoblasts, and we found that 100 µM CoCl2 was appropriate to treat osteoblasts for 48 hours. The analysis of flow cytometer showed that CoCl2-treated osteoblasts apoptosis can be ameliorated when cocultured with BMSCs-EVs. Further findings revealed that reactive oxygen species (ROS) was related to CoCl2-induced apoptosis. In addition, our results demonstrated that EVs exerted an important role in increasing expression levels of ALP, BMP-2, OCN, and OSTERIX under hypoxia. Similarly, the functional effects of BMSCs-EVs were observed on the osteoblasts mineralization. In summary, these findings provide insight that BMSCs-EVs might decrease the effect of CoCl2-induced apoptosis through inhibiting ROS, and promote osteogenic differentiation under hypoxia.

Bifunctional Ultrathin RhRu0.5 -Alloy Nanowire Electrocatalysts for Hydrazine-Assisted Water Splitting.

Hydrazine-assisted water electrolysis offers a feasible path for low-voltage green hydrogen production. Herein, the design and synthesis of ultrathin RhRu0.5 -alloy wavy nanowires as bifunctional electrocatalysts for both the anodic hydrazine oxidation reaction (HzOR) and the cathodic hydrogen evolution reaction (HER) is reported. It is shown that the RhRu0.5 -alloy wavy nanowires can achieve complete electrooxidation of hydrazine with a low overpotential and high mass activity, as well as improved performance for the HER. The resulting RhRu0.5 bifunctional electrocatalysts enable, high performance hydrazine-assisted water electrolysis delivering a current density of 100 mA cm-2 at an ultralow cell voltage of 54 mV and a high current density of 853 mA cm-2 at a cell voltage of 0.6 V. The RhRu0.5  electrocatalysts further demonstrate a stable operation at a high current density of 100 mA cm-2 for 80 hours of testing period with little irreversible degradation. The overall performance greatly exceeds that of the previously reported hydrazine-assisted water electrolyzers, offering a pathway for efficiently converting hazardous hydrazine into molecular hydrogen.

Prognostic value of Musashi 2 (MSI2) in cancer patients: A systematic review and meta-analysis.

Musashi 2 (MSI2) is an RNA-binding protein that regulates mRNA translation of numerous intracellular targets and plays an important role in the development of cancer. However, the prognostic value of MSI2 in various cancers remains controversial. Herein, we conducted this meta-analysis including 21 studies with 2640 patients searched from PubMed, Web of Science, EMBASE, Chinese National Knowledge Infrastructure databases, and WanFang databases to accurately assess the prognostic significance of MSI2 in various cancers. Our results indicated that high MSI2 expression was significantly related to poor overall survival (HR = 1.84, 95% CI: 1.66-2.05, P < 0.001) and disease-free survival (HR = 1.73, 95% CI: 1.35-2.22, P < 0.001). In addition, MSI2 positive expression was associated with certain phenotypes of tumor aggressiveness, such as clinical stage, depth of invasion, lymph node metastasis, liver metastasis and tumor size. In conclusion, elevated MSI2 expression is closely correlated with poor prognosis in various cancers, and may serve as a potential molecular target for cancer patients.

Inhibitory effects of Rap1GAP overexpression on proliferation and migration of endothelial cells via ERK and Akt pathways.

Rap1 is expressed in human umbilical vein endothelial cells (HUVECs). Rap1-GTPase activating protein (Rap1GAP), with its specific target, Rap1, has been shown to be important in the regulation of many physiological and certain pathological processes. In this study, we investigated the effect of Rap1GAP expression on endothelial cell function, or, more specifically, proliferation and migration of endothelial cells. HUVECs were transfected with pcDNA3.1 (empty vector), pcDNA3.1 containing Flag-tagged-Rap1GAP or Myc-tagged-Rap1N17. The proliferation, migration and tube formation were examined and compared among the 3 groups. Expression of Rap1, Rap1GAP, extracellular signal-regulated kinase (ERK), phospho-ERK, Akt, phosphor-Akt was detected by Western blotting. The results showed that the proliferation, migration and tube formation were significantly reduced in Rap1GAP- and Rap1N17-transfected HUVECs as compared with empty vector-transfected control. These changes were coincident with increased expression of Rap1GAP and decreased expression of activated Rap1, phospho-ERK and -Akt. After treatment of Rap1GAP-transfected HUVECs with a stimulator of Rap1 guanine-nucleotide-exchange factor (Rap1GEF) 8CPT-2'OMe-cAMP, it was found that Rap1 activity was decreased as compared with empty vector-transfected control. Pretreatment of HUVECs with an ERK inhibitor PD98059 or a PI3K inhibitor LY294002 prior to stimulation not only blocked 8CPT-2'OMe-cAMP-induced phosphorylation of ERK and Akt, but also significantly reduced cell proliferation and migration. Finally, we examined the effect of vascular endothelial growth factor (VEGF) on HUVECs overexpressing Rap1GAP. VEGF-stimulated Rap1 activity, phosphorylation of ERK and Akt, cyclin D1 expression and cell proliferation were repressed in HUVECs overexpressing Rap1GAP as compared to empty vector-transfected control. Taken together, our findings demonstrate that Rap1GAP/Rap1 and their downstream effectors regulate proliferation and migration of HUVECs via ERK and Akt pathways.

MicroRNA-21 mediates the protective role of emulsified isoflurane against myocardial ischemia/reperfusion injury in mice by targeting SPP1.

Isoflurane has demonstrated to exert protective impacts against ischemia/reperfusion (I/R) injury in some organs. This research explored the role of emulsified isoflurane (EI) in myocardial I/R injury through the interaction with microRNA-21 (miR-21). The myocardial I/R injury mouse models established by coronary artery ligation were respectively treated with EI, miR-21 mimic/inhibitor or silenced secreted phosphoprotein 1 (SPP1) plasmids. Then, the pathology, fibrosis and cardiomyocyte apoptosis in mouse myocardial tissues were observed. Furthermore, the expression levels of miR-21, SPP1, oxidative stress indices, inflammatory factors and apoptotic proteins in mouse myocardial tissues were determined. The targeting relation between miR-21 and SPP1 was confirmed. MiR-21 was poorly expressed and SPP1 was highly expressed in myocardial I/R injury mice. EI treatment, elevated miR-21, or silenced SPP1 improved cardiac function and suppressed the oxidative stress, myocardial fibrosis, inflammatory reaction and cardiomyocyte apoptosis in myocardial I/R injury mice, thereby reliving the myocardial I/R injury. These therapeutic effects of EI were repressed by miR-21 inhibition. Additionally, SPP1 was targeted by miR-21. Results in our research indicated that miR-21 mediated the therapeutic effect of EI on myocardial I/R injury in mice by targeting SPP1. This study may provide a novel treatment strategy for myocardial I/R injury.

The predictive value of galectin-1 and vascular mimicry in the prognostic evaluation of patients with rectal cancer.

BACKGROUND: This study aims to investigate the expression of galectin-1 and vascular mimicry (VM) in rectal cancer tissues, and to assess their predictive value in the prognostic evaluation of patients with rectal cancer. METHODS: Immunohistochemistry (IHC) and CD34-periodic acid solution (PAS) double staining were used to detect galectin-1 expression and the formation of VM in rectal cancer tissues from 94 patients with stage I-III rectal cancer and their corresponding paracancerous tissues. We also analyzed the relationship between the expression of galectin-1, VM, various clinicopathological parameters, and the prognosis of rectal cancer patients, as well as their influence on the overall survival (OS) of rectal cancer patients. RESULTS: Among the 94 tissue specimens from rectal cancer patients, 43 had positive expression of galectin-1 and 19 had positive expression of VM. There was a positive correlation between VM and galectin-1 expression in rectal cancer tissue. Galectin-1 expression in rectal cancer tissue and the formation of VM were related to tumor differentiation, staging, lymph node metastasis, and intravascular tumor thrombus (P<0.05). Kaplan-Meier analysis showed that the OS time of rectal cancer patients in the galectin-1 positive expression group was shorter than the galectin-1 negative expression patients, and the difference between the 2 groups was statistically significant (P=0.003). The OS time of patients with rectal cancer in the VM positive expression group was shorter than the VM negative expression group, and the difference between the two groups was statistically significant (P<0.001). The OS time of the galectin-1 and VM negative expression group was 57.33±1.13 months, and the OS time of the galectin-1 and VM positive expression group was 43.21±3.97 months, while the OS time of the galectin-1 positive expression and VM negative expression group was 55.42±2.23 months, and the difference between the three groups was statistically significant (P<0.001). Multi-factor analysis results indicated that invasion depth and VM expression were independent risk factors that affected the OS of patients with rectal cancer. CONCLUSIONS: Galectin-1 and VM expression in rectal cancer tissues may predict poor prognosis in patients after radical surgery. Galectin-1 and VM may therefore become potential new targets for rectal cancer treatment.

LncRNA Xist induces arterial smooth muscle cell apoptosis in thoracic aortic aneurysm through miR-29b-3p/Eln pathway.

BACKGROUND: Thoracic aortic aneurysm (TAA) is a serious disease usually happening in elder people and with high death rate. Accumulating studies have reported that long non-coding RNAs (lncRNAs) are implicated in the progression of various human diseases, including TAA. AIM: In our study, we intended to explore the function of elastin (Eln) and its upstream mechanism in TAA. METHODS: RT-qPCR determined gene expressions and western blot tested changes in protein levels. Ang Ⅱ treatment was implemented to induce cell apoptosis. Flow cytometry analysis, TUNEL assay and JC-1 assay were exploited to measure cell apoptosis. Meanwhile, mechanistic assays such as RIP, RNA pull down and luciferase reporter assays were employed to identify the interplay between RNAs. RESULTS: Eln inhibition was identified to protect rat arterial smooth muscle cells from apoptosis. Also, miR-29b-3p was identified to bind to Eln, and X inactive specific transcript (Xist) could boost Eln expression through absorbing miR-29b-3p. Meanwhile, Eln overexpression counteracted the suppression of silenced Xist on the apoptosis of rat arterial smooth muscle cells. More importantly, such ceRNA network was proved to aggravate the apoptosis of human aortic smooth muscle cells. CONCLUSION: LncRNA Xist contributes to arterial smooth muscle cell apoptosis through miR-29b-3p/Eln pathway, providing new potential roads for treating TAA.

Characterization of a Novel Hepatitis C Subtype, 6xj, and Its Consequences for Direct-Acting Antiviral Treatment in Yunnan, China.

Hepatitis C virus (HCV) has a high rate of genetic variability, with eight genotypes and 91 subtypes. The genetic diversity of HCV genotype 6 (HCV-6) is the highest with 31 subtypes, and this genotype is prevalent in Southeast Asia. In this study, we investigated 160 individuals with chronic hepatitis C in Yunnan Province, China. Using reverse transcription (RT)-PCR and Sanger sequencing, 147 cases were successfully amplified and genotyped as 3b (4.9%), 3a (19.73%), 6n (12.24%), 1b (7.48%), 2a (6.12%), 6a (2.04%), 1a (0.68%), 6v (0.68%), and 6xa (0.68%), with eight sequences remaining unclassified. Subsequently, the eight nearly full-length genomes were successfully amplified and analyzed. The eight complete coding sequences formed a phylogenetic group that was distinct from the previously assigned HCV-6 subtypes and clustered with two previously unnamed HCV-6 sequences. Furthermore, Simplot analysis showed no recombination and the p-distance was more than 15% in comparison to the 6a to 6xi subtypes. Taken together, we identified a new HCV-6 subtype, 6xj, which originated approximately in 1775 according to Bayesian analyses. Moreover, all eight individuals received follow-up assessments at 44 weeks from the beginning of their 12-week treatments of sofosbuvir/velpatasvir (after-treatment week 32). One case relapsed at after-treatment week 32. Next-generation sequencing (NGS) was conducted and showed that the treatment failure case had two suspected antiviral resistance mutations, NS5A V28M (a change of V to M at position 28) and NS5B A442V, compared with the baseline. Overall, this newly identified 6xj subtype further confirmed the high diversity of the HCV-6 genotype. The newly identified resistance-associated amino acid substitutions may help inform future clinical treatments. IMPORTANCE This study investigated the genetic diversity of hepatitis C virus (HCV), particularly in relation to genotype 6, which is prevalent in Yunnan, China, and is often difficult to treat successfully. We identified a new HCV-6 subtype, 6xj, which is an ancient strain. Moreover, all eight individuals with the novel subtype received follow-up assessments at 44 weeks from the beginning of their treatments. One case relapsed after 8 months of withdrawal. NGS was conducted and showed that the isolate from the treatment failure case had two suspected antiviral resistance mutations, NS5A V28M and NS5B A442V, compared with the baseline. Overall, this newly identified 6xj subtype further confirmed the high diversity of the HCV-6 genotype. The newly identified resistance-associated amino acid substitutions may help inform future clinical treatments. We believe that our study makes a significant contribution to the literature based on the results described above.

Silver nanoparticles boost charge-extraction efficiency in Shewanella microbial fuel cells.

Microbial fuel cells (MFCs) can directly convert the chemical energy stored in organic matter to electricity and are of considerable interest for power generation and wastewater treatment. However, the current MFCs typically exhibit unsatisfactorily low power densities that are largely limited by the sluggish transmembrane and extracellular electron-transfer processes. Here, we report a rational strategy to boost the charge-extraction efficiency in Shewanella MFCs substantially by introducing transmembrane and outer-membrane silver nanoparticles. The resulting Shewanella-silver MFCs deliver a maximum current density of 3.85 milliamperes per square centimeter, power density of 0.66 milliwatts per square centimeter, and single-cell turnover frequency of 8.6 × 105 per second, which are all considerably higher than those of the best MFCs reported to date. Additionally, the hybrid MFCs feature an excellent fuel-utilization efficiency, with a coulombic efficiency of 81%.

Arylaminomethyl Radical-Initiated Cascade Annulation Reaction of Quinoxalin-2(1H)-ones Catalyzed by Recyclable Photocatalyst Perovskite.

A feasible arylaminomethyl radical-triggered tandem annulation reaction has been developed toward a large variety of poly fused heterocycles, tetrahydroimidazo[1,5-a]quinoxalin-4(5H)-ones, by reacting diverse quinoxalin-2(1H)-ones with various N-arylglycines in green solvent (DMC) in the presence of CsPbBr3 under white-light irradiation conditions.

Endothelial HuR deletion reduces the expression of proatherogenic molecules and attenuates atherosclerosis.

Atherosclerosis is a chronic inflammatory disease of arterial wall, and the proatherogenic molecules derived from endothelium and leukocyte recruitment are major contributors to its pathogenesis. The RNA-binding protein HuR plays several physiological roles in endothelial cells, but its relevance to atherosclerosis is not yet determined. Here, by utilizing the ApoE-/- mice depleted of endothelia HuR (ApoE-/-; HuRfl/fl; Cdh5-Cre), we observed that these mice exhibited attenuated atherosclerosis compared with wild-type littermates (ApoE-/-; HuRfl/fl). Mechanistically, this phenomenon may not be associated with systemic effects on lipid metabolism, however, we found that the expression levels of proatherogenic molecules, degree of local inflammation and extent of leukocyte recruitment to aortic endothelium were all decreased when endothelia HuR was absent. Collectively, our study uncovers the role of endothelia HuR deletion in attenuating atherosclerosis, and suggests that this effect is at least in part attributed to the decreased expression of proatherogenic molecules and suppressed local inflammation. Hence, our study might offer a potential strategy for atherosclerosis treatment via manipulating endothelia HuR.

Interleukin-6 (IL-6) triggers the malignancy of hemangioma cells via activation of HIF-1α/VEGFA signals.

Hemangioma (HA) is tumor formed by hyper-proliferation of vascular endothelial cells. The roles of interleukins on the progression of HA are not well illustrated. Our present study revealed that the expression of interleukin -6 (IL-6) and IL-8 in HA cells were significantly increased as compared with that in the human umbilical vein endothelial cell (HUVEC) cells. Targeted inhibition of IL-6, while not IL-8, can significantly suppress the proliferation and migration of HA cells. IL-6 treatment can increase the expression of vascular endothelial growth factor A (VEGFA), while had no significant effect on the expression of basic fibroblast growth factor (bFGF), in HA cells. Deletion of VEGFA can abolish IL-6 induced progression of HA, suggesting the essential role of VEGFA in IL-6 induced HA development. The specific inhibitor of hypoxia-inducible factor (HIF)-1α, while not Sp1, NF-κB, or AP1, abolished IL-6 induced VEGFA expression. Over expression of HIF-1α can attenuate anti-IL-6 suppressed expression of VEGFA in HA cells. Furthermore, IL-6 triggered the expression, nuclear translocation, and transcription activities of HIF-1α in HA cells via increasing its binding with the signal transducer and activator of transcription-3 (STAT3). STAT3 inhibitor CPA7 or si-STAT3 can abolish IL-6 induced upregulation of HIF-1α in HDEC cells. Collectively, our study revealed that IL-6 can trigger the malignancy of HA cells via induction of proliferation and migration. The activation of STAT3/HIF-1α/VEGFA signal was essential for this process. It suggested that IL-6/STAT3/HIF-1α/VEGFA signal may represent a novel therapeutic target for human HA treatment.

Limb graft occlusion following endovascular aortic repair: Incidence, causes, treatment and prevention in a study cohort.

The present study investigated the incidence, causes, treatment and prevention of limb graft occlusion following endovascular aortic repair (EVAR). A total of 66 cases of abdominal aortic aneurysm receiving EVAR at our department from January 2005 to December 2013 were enrolled. After EVAR, patients received routine antiplatelet therapy of 75 mg PLAVIX for 6 months and then 100 mg Aspirin for another 6 months by oral administration. According to previous clinical experiences, antiplatelet therapy is able to effectively reduce the incidence of iliac occlusion after EVAR. A total of 61 bifurcated grafts and 5 aortauniilac grafts (127 limbs in total) were used. Physical examination, ankle-brachial-index and computer tomographic angiography were performed at 10 days, at 3, 6 and 12 months and annually thereafter. It was found that 7 limbs in 7 patients (10.6% of patients, 5.5% of limbs) were occluded between 20 days and 12 months (average, 7.8±5.3 months) after EVAR. Acute and severe ischemia was found in 2 cases, claudication was in found 3 cases, asthenia in both legs was found in 1 case and 1 case was asymptomatic. Femoral-femoral bypass, femoral-femoral bypass and stenting, aorto-iliac/femoral bypass, thrombectomy and conservative treatment were performed in 1 patient each and thrombectomy together with stenting was performed in 2 cases. Limb graft occlusion was not rare after EVAR. Treatment of this complication included surgery and endovascular therapy such as bypass, thrombectomy and thrombolysis. In conclusion, aggressive pre-emptive treatment including angioplasty and stenting prevented occlusion in certain cases.