Ligand-Functionalized MIL-68-type Indium(III) Metal-Organic Frameworks with Prominent Intrinsic Proton Conductivity.

Indium-based metal-organic frameworks (In-MOFs) have now become an attractive class of porous solids in materials science and electrochemistry due to their diverse structures and promising applications. In the field of proton conduction, to find more crystalline MOFs with splendid proton-conductive properties, herein, five three-dimensional isostructural In-MOFs, MIL-68-In or MIL-68-In-X (X = NH2, OH, Br, or NO2) using terephthalic acid (H2BDC) or functionalized terephthalic acids (H2BDC-X) as multifunctional linkages were efficiently fabricated. First, the outstanding structural stability of the five MOFs, including thermal and water stability, was verified by thermal analysis and powder X-ray diffraction. Subsequently, the H2O-mediated proton conductivities (σ) were fully assessed and compared. Notably, their σ evinced a significant positive correlation between the temperature or relative humidity (RH) and varied with the functional groups on the organic ligands. Impressively, their highest σ values are up to 10-3-10-4 S/cm (100 °C/98% RH) and change in this order: MIL-68-In-OH (1.72 × 10-3 S/cm) > MIL-68-In-NH2 (1.70 × 10-3 S/cm) > MIL-68-In-NO2 (4.47 × 10-4 S/cm) > MIL-68-In-Br (4.11 × 10-4 S/cm) > MIL-68-In (2.37 × 10-4 S/cm). Finally, the computed activation energy values under 98 or 68% RHs are assessed, and the related proton conduction mechanisms are speculated. Moreover, after electrochemical testing, these MOFs illustrate remarkable structural rigidity, laying a meritorious material foundation for future applications.

Risk Factors of Acute Pain in Elderly Patients After Laparoscopic Radical Resection of Colorectal Cancer.

OBJECTIVE: To investigate the risk factors of acute pain after laparoscopic radical resection of colorectal cancer (CRC) in elderly patients. METHODS: Totally, 143 elderly patients (≥ 60 y old) who received laparoscopic radical resection of CRC in the People's Hospital of Xinjiang Uygur Autonomous Region from March 2021 to August 2022 were retrospectively analyzed. The patients were divided into 2 groups according to visual analog scale (VAS) scores 24 h after surgery: mild pain group (VAS score ≤ 3, n=108) and moderate to severe pain group (VAS score >3, n=35). The data of the patients, including sex, age, height, body mass, intraoperative blood loss, intraoperative urine volume, intraoperative opioid dosage, operation duration, preoperative Hospital Anxiety and Depression Scale (HADS) scores, preoperative Mini-Mental State Examination scores, VAS scores, postoperative nausea and vomiting scores were recorded. Multivariate logistic regression analysis was used to screen the risk factors of postoperative acute pain in elderly patients undergoing laparoscopic radical resection of CRC. RESULTS: The preoperative HADS score of the moderate to severe pain group was significantly increased compared with that of the mild pain group (10.8±2.4 vs. 6.2±1.9), as well as the operation duration (226.4±18.3 vs. 186.1±12.7), the intraoperative dosage of remifentanil (3.7±0.2 vs. 3.2±0.4), the preoperative VAS score [4(2, 7) vs. 2 (0, 4)] and postoperative VAS score [5 (4, 6) vs. 3 (2, 3)] ( P <0.05). Multivariate logistic regression analysis showed that high preoperative HADS score, long operation duration, and high preoperative VAS score ( P <0.05) were independent risk factors for acute pain after laparoscopic radical resection of CRC in elderly patients. CONCLUSION: Preoperative anxiety and depression, preoperative pain, and long operation duration are risk factors for acute pain in elderly patients after laparoscopic radical resection of CRC.

The growth inhibitory effects and non-targeted metabolomic profiling of Microcystis aeruginosa treated by Scenedesmus sp.

The health of the aquatic ecosystem has recently been severely affected by cyanobacterial blooms brought on by eutrophication. Therefore, it is critical to develop efficient and secure methods to control dangerous cyanobacteria, such as Microcystis aeruginosa. In this research, we tested the inhibition of M. aeruginosa growth by a Scenedesmus sp. strain isolated from a culture pond. Scenedesmus sp. culture filtrate that had been lyophilized was added to M. aeruginosa, and cultivation for seven days, the cell density, chlorophyll a (Chl-a) concentration, maximum quantum yield of photosystem II (Fv/Fm), the activities of superoxide dismutase (SOD), catalase (CAT), and the concentration of malondialdehyde (MDA) and glutathione (GSH) were measured. Moreover, non-targeted metabolomics was carried out to provide light on the inhibitory mechanism in order to better understand the metabolic response. According to the results, M. aeruginosa is effectively inhibited by the lyophilized Scenedesmus sp. culture filtrate at a rate of 51.2%. Additionally, the lyophilized Scenedesmus sp. clearly inhibit the photosystem and damages the antioxidant defense system of M. aeruginosa cells, resulting in oxidative damage, which worsens membrane lipid peroxidation, according to changes in Chl-a, Fv/Fm, SOD, CAT enzyme activities and MDA, GSH. Metabolomics analysis revealed that the secondary metabolites of Scenedesmus sp. significantly interfere with the metabolism of M. aeruginosa involved in amino acid synthesis, membrane creation and oxidative stress, which is coherent with the morphology and physiology outcomes. These results demonstrate that the secondary metabolites of Scenedesmus sp. exert algal inhibition effect by breaked the membrane structure, destroyed the photosynthetic system of microalgae, inhibited amino acid synthesis, reduced antioxidant capacity, and eventually caused algal cell lysis and death. Our research provides a reliable basis for the biological control of cyanobacterial blooms on the one hand, and on other hand supply application of non-targeted metabolome on the study of microalgae allelochemicals.

Nrf2 protects against myocardial ischemia-reperfusion injury in diabetic rats by inhibiting Drp1-mediated mitochondrial fission.

Mitochondrial dysfunction and oxidative stress are considered to be two main drivers of diabetic myocardial ischemia-reperfusion injury (DM + MIRI). Nuclear factor-erythroid 2-related factor 2 (Nrf2) and Dynamin-related protein 1 (Drp1) play central roles in maintaining mitochondrial homeostasis and regulating oxidative stress, but the effects of the Nrf2-Drp1 pathway on DM-MIRI have not been reported. The aim of this study is to investigate the role of the Nrf2-Drp1 pathway in DM + MIRI rats. A rat model of DM + MIRI and H9c2 cardiomyocyte injury were constructed. The therapeutic effect of Nrf2 was assessed by detecting myocardial infarct size, mitochondrial structure, levels of myocardial injury markers and oxidative stress, apoptosis, and Drp1 expression. The results showed that DM + MIRI rats had increased myocardial infarct size and Drp1 expression in myocardial tissue, accompanied by increased mitochondrial fission and oxidative stress. Interestingly, Nrf2 agonist dimethyl fumarate (DMF) could significantly improve cardiac function, mitochondrial fission, and decrease oxidative stress levels and Drp1 expression after ischemia. However, these effects of DMF would be largely counteracted by the Nrf2 inhibitor ML385. Additionally, Nrf2 overexpression significantly suppressed Drp1 expression, apoptosis, and oxidative stress levels in H9c2 cells. Nrf2 attenuates myocardial ischemia-reperfusion injury in DM rats by reducing Drp1-mediated mitochondrial fission and oxidative stress.

[Pharmacodynamic material basis and anti-inflammatory mechanism of Chrysanthemum morifolium cv. Fubaiju based on UPLC-Q-TOF-MS/MS combined with network pharmacology].

The chemical components in rats after oral administration of the water extract of Chrysanthemum morifolium cv. Fubaiju(CMF) were analyzed by UPLC-Q-TOF-MS/MS technique. Forty-four compounds were identified from the water extract of CMF and 11 components were identified from the rat serum. A total of 264 potential anti-inflammatory targets were identified by network pharmacology based on serum components. The "component-target" network and protein-protein interaction(PPI) network were constructed, and GO function enrichment and KEGG pathway enrichment analyses were performed. The molecular docking was carried out to validate the results of network pharmacology. The results showed that CMF might act on AKT1, TNF, TP53, IL6, INS, and other core targets through apigenin, luteolin, acacetin, diosmetin, 3,4-O-dicaffeoylquinic acid, and other active components, and exert anti-inflammatory effects by regulating PI3 K-AKT signaling pathway, FoxO signaling pathway, cAMP signaling pathway, Ras signaling pathway, and other pathways. The pharmacodynamic materials basis of CMF was identified by UPLC-Q-TOF-MS/MS technology, and the core anti-inflammatory targets and the underlying mechanism of action were analyzed by network pharmacology and molecular docking, which provided a reference for comprehensively clarifying the pharmacodynamic materials basis and quality control of CMF.

Ghrelin infusion into the basolateral amygdala suppresses CTA memory formation in rats via the PI3K/Akt/mTOR and PLC/PKC signaling pathways.

Ghrelin is a circulating orexigenic hormone that promotes feeding behavior and regulates metabolism in humans and rodents. We previously reported that local infusion of ghrelin into the basolateral amygdala (BLA) blocked memory acquisition for conditioned taste aversion (CTA) by activating growth hormone secretagogue receptor 1a. In this study, we further explored the underlying mechanism and signaling pathways mediating ghrelin modulation of CTA memory in rats. Pharmacological agents targeting distinct signaling pathways were infused into the BLA during conditioning. We showed that preadministration of the PI3K inhibitor LY294002 abolished the repressive effect of ghrelin on CTA memory. Moreover, LY294002 pretreatment prevented ghrelin from inhibiting Arc and zif268 mRNA expression in the BLA triggered by CTA memory retrieval. Preadministration of rapamycin eliminated the repressive effect of ghrelin, while Gsk3 inhibitors failed to mimic ghrelin's effect. In addition, PLC and PKC inhibitors microinfused in the BLA blocked ghrelin's repression of CTA acquisition. These results demonstrate that ghrelin signaling in the BLA shapes CTA memory via the PI3K/Akt/mTOR and PLC/PKC pathways. We conducted in vivo multichannel recordings from mouse BLA neurons and found that microinjection of ghrelin (20 µM) suppressed intrinsic excitability. By means of whole-cell recordings from rat brain slices, we showed that bath application of ghrelin (200 nM) had no effect on basal synaptic transmission or synaptic plasticity of BLA pyramidal neurons. Together, this study reveals the mechanism underlying ghrelin-induced interference with CTA memory acquisition in rats, i.e., suppression of intrinsic excitability of BLA principal neurons via the PI3K/Akt/mTOR and PLC/PKC pathways.

Experimental and clinical evidence suggests that GRPEL2 plays an oncogenic role in HCC development.

Hepatocellular carcinoma (HCC) continues to cause severe burden worldwide. The limited options especially toward HCC with metastasis prompts us to identify novel molecules for either diagnostic/prognostic or therapeutic purposes. GRPEL2 is well defined in maintaining mitochondrial homeostasis, which is critical to multiple biological processes for cancer survival. However, its role in HCC progression was not investigated before. In our analysis using data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA LIHC) dataset and tissue microarray, higher expression levels of GRPEL2 were obseved in HCC tissues compared to in normal liver tissues, and indicated higher tumor grade, higher tumor stage, and shorter overall survival (OS). Consistent with the results of above analyses, the functional experiments validated that GRPEL2 acted as a tumor-promoting factor in HCC progression. GRPEL2 knockdown suppressed cell growth, migration, and invasion in vitro, as well as inhibited tumor growth in vivo. Moreover, GRPEL2 deficiency also accelerated reactive oxygen species (ROS) production and increased mitochondrial membrane potential (MMP), leading to cell apoptosis. In addition, we found that the cell cycle and NF-κB signaling pathways were responsible for GRPEL2-induced HCC progression, based on the results of Gene Set Enrichment Analysis (GSEA) and subsequent experimental validation. Our study, for the first time, identified the role of GRPEL2 in HCC development and provided a compelling biomarker for targted therapy in HCC treatment.

Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.

Vascular endothelial dysfunction is associated with the progress of many diseases. Circular RNAs (circRNAs) take part in the dysfunction of vascular endothelium. CircRNA hsa_circ_0008360 (circ_0008360) is dysregulated in high glucose-treated vascular endothelium, while the role and mechanism of circ_0008360 in high glucose-induced dysfunction remain unknown. Human umbilical vascular endothelium cells (HUVEC) were stimulated via high glucose. The abundances of circ_0008360, miR-186-5p and cyclin D2 (CCND2) were examined via quantitative real-time polymerase chain reaction or western blot. Vascular endothelial dysfunction was assessed via cell viability, apoptosis, migration and tube formation. The target relationship between miR-186-5p and circ_0008360 or CCND2 was analyzed via dual-luciferase reporter, RNA pull-down and RNA immunoprecipitation analyses. Circ_0008360 expression was enhanced in high-glucose-treated HUVEC. Circ_0008360 silence mitigated high glucose-induced suppression of viability, migration, tube formation, and increase in apoptosis in HUVEC. MiR-186-5p was sponged by circ_0008360, and miR-186-5p inhibition reversed the effect of circ_0008360 silence on high glucose-induced vascular endothelial dysfunction. MiR-186-5p alleviated high glucose-induced vascular endothelial dysfunction via targeting CCND2. CCND2 interference abolished the aggravated effect of circ_0008360 on high glucose-induced vascular endothelial dysfunction. Circ_0008360 knockdown attenuated high glucose-induced vascular endothelial dysfunction via regulating miR-186-5p and CCND2, indicating circ_0008360 might act as a target for the treatment of vascular endothelial dysfunction.Abbreviations: circRNAs, circular RNAs; HUVEC, human umbilical vascular endothelium cells; CCND2, cyclin D2; XPNPEP3, X-prolyl aminopeptidase 3; ceRNAs, competing endogenous RNAs; miRNAs, microRNAs; qRT-PCR, quantitative real-time polymerase chain reaction; RIP, RNA immunoprecipitation; HIF-1α, hypoxia inducible factor 1 alpha; TLR3, toll-like receptor 3; AKAP12, A-Kinase Anchoring Protein 12; ox-LDL, oxidized low-density lipoprotein; HG, high glucose; NG, normal glucose.

LncRNA SNHG15 relieves hyperglycemia-induced endothelial dysfunction via increased ubiquitination of thioredoxin-interacting protein.

Numerous studies have revealed that hyperglycemia is a pivotal driver of diabetic vascular complications. However, the mechanisms of hyperglycemia-induced endothelial dysfunction in diabetes remain incompletely understood. This study aims to expound on the underlying mechanism of the endothelial dysfunction induced by hyperglycemia from the perspective of long non-coding RNAs (lncRNA). In this study, a downregulation of SNHG15 was observed in the ischemic hind limb of diabetic mice and high glucose (HG)-treated HUVECs. Functionally, the overexpression of SNHG15 promoted cell proliferation, migration, and tube formation, and suppressed cell apoptosis in HG-treated HUVECs. Mechanistically, SNHG15 reduced thioredoxin-interacting protein (TXNIP) expression by enhancing ITCH-mediated ubiquitination of TXNIP. TXNIP overexpression abrogated the protective effect of lncRNA SNHG15 overexpression on HG-induced endothelial dysfunction. The following experiment further confirmed that SNHG15 overexpression promoted angiogenesis of the ischemic hind limb in diabetic mice. In conclusion, SNHG15 is a novel protector for hyperglycemia-induced endothelial dysfunction via decreasing TXNIP expression.

The prevalence of fatigue among Chinese nursing students in post-COVID-19 era.

BACKGROUND: Due to the COVID-19 outbreak, all teaching activities in nursing schools were suspended in China, and many nursing students were summoned to work in hospitals to compensate for the shortage of manpower. This study examined the prevalence of fatigue and its association with quality of life (QOL) among nursing students during the post-COVID-19 era in China. METHODS: This was a multicenter, cross-sectional study. Nursing students in five Chinese universities were invited to participate. Fatigue, depressive and anxiety symptoms, pain and QOL were measured using standardized instruments. RESULTS: A total of 1,070 nursing students participated. The prevalence of fatigue was 67.3% (95% CI [64.4-70.0]). Multiple logistic regression analysis revealed that male gender (P = 0.003, OR = 1.73, 95% CI [1.20-2.49]), and being a senior nursing student (second year: OR = 2.20, 95% CI [1.46-3.33], P < 0.001; third year: OR = 3.53, 95% CI [2.31-5.41], P < 0.001; and fourth year OR = 3.59, 95% CI [2.39-5.40], P < 0.001) were significantly associated with more severe fatigue. In addition, moderate economic loss during the COVID-19 pandemic (OR = 1.48, 95% CI [1.08-3.33], P < 0.015; compared to low loss), participants with more severe depressive (OR = 1.48, 95% CI [1.22-1.78], P < 0.001) and anxiety symptoms (OR = 1.12, 95% CI [1.05-1.20], P = 0.001), and more severe pain (OR = 1.67, 95%CI [1.46-1.91], P < 0.001) were significantly associated with reported more severe fatigue. After controlling for covariates, nursing students with fatigue had a lower overall QOL score compared to those without (F (1, 1070) = 31.4, P < 0.001). CONCLUSION: Fatigue was common among nursing students in the post-COVID-19 era. Considering the negative impact of fatigue on QOL and daily functioning, routine physical and mental health screening should be conducted for nursing students. Effective stress-reduction measures should be enforced to assist this subpopulation to combat fatigue and restore optimal health.

LncRNA SNHG15 relieves hyperglycemia-induced endothelial dysfunction via increasing ubiquitination of thioredoxin-interacting protein.

OBJECTIVE: Numerous evidence indicates that hyperglycemia is a pivotal driver of the vascular complications of diabetes. However, the mechanisms of hyperglycemia-induced endothelial dysfunction in diabetes remain incompletely understood. This study aims to expound on the underlying mechanism of the endothelial dysfunction induced by hyperglycemia from the perspective of long non-coding RNAs (lncRNA). MATERIALS AND METHODS: Cell proliferation, migration, apoptosis, and tube formation were measured by cell counting kit-8 assay, transwell assay, flow cytometry, and tube formation assay, respectively. RNA pull-down and RNA-binding protein immunoprecipitation were used to detect the interaction between lncRNA SNHG15 and thioredoxin-interacting protein (TXNIP). Co-immunoprecipitation was used to detect the ubiquitination level of TXNIP and the interaction between TXNIP and E3 ubiquitin ligase ITCH. RESULTS: A downregulation of SNHG15 was observed in the ischemic hind limb of diabetic mice and high glucose (HG)-treated HUVECs. Functionally, the overexpression of SNHG15 promoted cell proliferation, migration, and tube formation, and suppressed cell apoptosis in HG-treated HUVECs. Mechanically, SNHG15 reduced TXNIP expression by enhancing ITCH-mediated ubiquitination of TXNIP. TXNIP overexpression abrogated the protective effect of LncRNA SNHG15 overexpression on HG-induced endothelial dysfunction. The following experiment further confirmed that SNHG15 overexpression promoted angiogenesis of the ischemic hind limb in diabetic mice. CONCLUSION: SNHG15 is a novel protector for hyperglycemia-induced endothelial dysfunction via decreasing TXNIP expression.

Proteasome activator PA200 maintains stability of histone marks during transcription and aging.

The epigenetic inheritance relies on stability of histone marks, but various diseases, including aging-related disorders, are usually associated with alterations of histone marks. Whether and how the proteasome is responsible for maintaining the histone marks during transcription and aging remain unclear. The core histones can be degraded by the atypical proteasome, which contains the proteasome activator PA200, in an acetylation-dependent manner during somatic DNA damage response and spermiogenesis. Methods: By utilizing a substitute of methionine to label proteins metabolically, we analyzed histone degradation genome-wide by sequencing the DNA fragments following pulse-chase assays. The genome-wide RNA-sequencing analysis was performed to analyze transcription and chromatin-immunoprecipitation (ChIP)-sequencing was used for analyses of histone marks. The experimental models included gene-manipulated cells (including both mouse and yeast), mouse liver, and mice. Results: Degradation of H4 or the transcription-coupled histone variant H3.3 could be suppressed by deletion of PA200 or its yeast ortholog Blm10. The histone deacetylase inhibitor accelerated the degradation rates of H3, while the mutations of the putative acetyl-lysine-binding region of PA200 abolished histone degradation in the G1-arrested cells. Deletion of PA200 dramatically altered deposition of the active transcriptional hallmarks (H3K4me3 and H3K56ac) and transcription, especially during cellular aging. Furthermore, deletion of PA200 or Blm10 accelerated cellular aging. Notably, the PA200-deficient mice displayed a range of aging-related deteriorations, including immune malfunction, anxiety-like behavior and shorter lifespan. Conclusion: PA200 promotes the transcription-coupled degradation of the core histones, and plays an important role in maintaining the stability of histone marks during transcription and aging.

Experimental Analysis of the Quality of Needle-Assisted Fenestration in Aortic Stent-Grafts and the Differences Between Gradual and Rapid Balloon Dilation.

Purpose: To report the findings of an in vitro experiment to evaluate the quality of needle fenestrations dilated by different size balloons in various stent-grafts and to investigate the differences between gradual and rapid dilation. Materials and Methods: Fenestrations were made using an 18-G needle in 5 different polyester or expanded polytetrafluoroethylene (ePTFE) stent-grafts: Relay, Valiant, Hercules, TAG, and Ankura. Each stent-graft received 2 groups of fenestrations: one was followed by gradual sequential dilation (4-, 6-, 8-, and 10-mm balloons) and the other by rapid dilation (4- and 10-mm balloons). The pressure was increased to 10 atmospheres or until the balloon was fully inflated with no waist. Quantitative and qualitative evaluations, including fenestration diameter, area, shape, and margins were conducted using light microscopy and scanning electron microscopy. Results: Relay had the strongest resistance to dilation and Ankura the slightest. The maximum length and area of holes expanded as the balloon diameter increased. The fenestrations in polyester devices were mostly elliptical or slit-like, with limited tears but extensive fibers visible in the margin, while ePTFE stent-grafts showed larger fenestration areas with clearer margins. Ankura showed the best quality of fenestrations, which were always circular or square without fabric tears, while the holes in the TAG were square or elliptical but sometimes had a slit after large balloon dilation (≥6 mm). The Relay, Valiant, Hercules, and Ankura devices showed no difference in maximum diameter, fenestration area, or scores of shape and margin (p>0.05). Rapid dilation in the TAG increased the rate of uncontrolled fabric tear, resulting in a larger final diameter (12.90 vs 10.82 mm, p=0.047), smaller area (30.46 vs 41.09 mm2, p=0.028), worse shape (0.75 vs 1.20, p=0.268), and worse margin (0.40 vs 1.00, p=0.174). Though the decreased fenestration shape and margin scores did not reach statistical significance, the trend for decline was more obvious than with the other devices. Conclusion: Materials and structures of the stent-grafts determine the quality of fenestrations dilated by different size balloons. The use of sequential vs rapid balloon dilation is also crucial for fashioning high-quality fenestrations and should be selected judiciously.

Long-term Results of Thoracic Endovascular Aortic Repair for Type B Aortic Dissection and Risk Factors for Survival.

Purpose: To compare characteristics of acute, subacute, and chronic type B aortic dissection and their influence on long-term results of thoracic endovascular aortic repair (TEVAR). Materials and Methods: In a single-center, retrospective cohort study, 314 patients (median age 52 years; 244 men) with acute (n=165), subacute (n=115), or chronic (n=34) type B aortic dissection underwent TEVAR between January 2009 and December 2013. Patient demographics, risk factors, and imaging characteristics were compared among the groups. Univariable and multivariable Cox regression analyses were performed to identify any factors influencing survival. Results: The acute and subacute patients exhibited more complications at presentation than chronic patients. However, the chronic patients exhibited more aneurysmal dilatation (p<0.001) and true lumen collapse (p<0.001). Over a mean follow-up of 68.1±22.9 months (range 2-108), subacute patients showed a lower reintervention rate (3.6% vs 12.1% vs 12.1%, p=0.045), a lower major complication rate (14.4% vs 33.1% vs 27.3%, p=0.002), and better cumulative overall survival (p=0.03) than the acute and chronic groups, respectively. Furthermore, acute patients developed more stent-graft-induced distal erosion (p=0.017) and retrograde type A dissection (RTAD) (p=0.036), whereas chronic patients had less aortic remodeling in the stented segment (p<0.001), distal thoracic aorta (p<0.001), and abdominal aorta (p=0.047). Finally, multivariable analysis demonstrated age >52 years, visceral malperfusion, and RTAD as independent factors influencing overall survival; aneurysmal dilatation, rupture/impending rupture, and RTAD were independent factors influencing aorta-specific survival. Conclusion: Acute and subacute patients had increased risks of rupture and complications at presentation, whereas chronic patients had increased risks for aneurysmal dilatation. From a long-term perspective, the subacute phase might be an optimal time for TEVAR in cases of type B aortic dissection that do not need emergent interventions. The risk factors influencing survival should be identified, carefully managed, and possibly prevented.

Design and Construction of a Metal-Organic Framework as an Efficient Luminescent Sensor for Detecting Antibiotics.

We first design and synthesize a dendritic aromatic 6-carboxyl linker (H6TDCPB), which is successfully assembled with Cd(II) ion to construct a porous metal-organic framework with a raw Cd6 cluster, {[Cd3(TDCPB)·2DMAc]·DMAc·4H2O}n (namely, complex 1). More interestingly, six adjacent linkers are packed together by π-π-stacking interactions to form an amazing six-molecule accumulation in the crystal structure. By virtue of high stability and luminescent properties, the as-synthesized sample not merely owns an excellent detectable ability but also possesses an outstanding selectivity for nitrofurans with remarkable recursitivity.

A Double-Walled Porous Metal-Organic Framework as a Highly Efficient Catalyst for Chemical Fixation of CO2 with Epoxides.

A double-walled MOF [Zn5(µ3-OH)2(DBTA)2(H2O)4]·solvents [1, H4DBTA = 2,2'-dihydroxy-1,1'-binaphthyl-3,3',6,6'-tetrakis(4-benzoic acid)] has been designed and constructed based on a rare Zn5 cluster. The resultant sample has enrichment of porous structure with high BET and Langmuir surface area. By virtue of multiaperture structure and plentiful catalytic sites of Brønsted (-OH) and Lewis acidic (ZnII), MOF 1 is a unique catalyst to synthesize cyclic carbonates from CO2 and epoxides with preferable repeatability.

SIP/CacyBP promotes autophagy by regulating levels of BRUCE/Apollon, which stimulates LC3-I degradation.

BRUCE/Apollon is a membrane-associated inhibitor of apoptosis protein that is essential for viability and has ubiquitin-conjugating activity. On initiation of apoptosis, the ubiquitin ligase Nrdp1/RNF41 promotes proteasomal degradation of BRUCE. Here we demonstrate that BRUCE together with the proteasome activator PA28γ causes proteasomal degradation of LC3-I and thus inhibits autophagy. LC3-I on the phagophore membrane is conjugated to phosphatidylethanolamine to form LC3-II, which is required for the formation of autophagosomes and selective recruitment of substrates. SIP/CacyBP is a ubiquitination-related protein that is highly expressed in neurons and various tumors. Under normal conditions, SIP inhibits the ubiquitination and degradation of BRUCE, probably by blocking the binding of Nrdp1 to BRUCE. On DNA damage by topoisomerase inhibitors, Nrdp1 causes monoubiquitination of SIP and thus promotes apoptosis. However, on starvation, SIP together with Rab8 enhances the translocation of BRUCE into the recycling endosome, formation of autophagosomes, and degradation of BRUCE by optineurin-mediated autophagy. Accordingly, deletion of SIP in cultured cells reduces the autophagic degradation of damaged mitochondria and cytosolic protein aggregates. Thus, by stimulating proteasomal degradation of LC3-I, BRUCE also inhibits autophagy. Conversely, SIP promotes autophagy by blocking BRUCE-dependent degradation of LC3-I and by enhancing autophagosome formation and autophagic destruction of BRUCE. These actions of BRUCE and SIP represent mechanisms that link the regulation of autophagy and apoptosis under different conditions.

An Exceptionally Stable TbIII-Based Metal-Organic Framework for Selectively and Sensitively Detecting Antibiotics in Aqueous Solution.

An exceptionally stable metal-organic framework based on one-dimensional (1D) TbIII chains with significant green emission under excitation energy, {[Tb(TATMA)(H2O)·2H2O} n (namely, 1), has been fabricated successfully under hydrothermal conditions. By virtue of the spectral overlap between the absorbance spectra of nitrofurans (NFAs) and the excitation spectrum of MOF 1, the resultant sample exhibits outstandingly sensitive and selective luminescence detectability for NFT ( Ksv = 3.35 × 104 M-1) and NFZ ( Ksv = 3.00 × 104 M-1) by quenching phenomenon. More importantly, it can detect NFAs in water from bovine serum samples. The portable MOF film can be easily prepared and used with excellent stability and recursitivity.

Rational Construction of an Exceptionally Stable MOF Catalyst with Metal-Adeninate Vertices toward CO2 Cycloaddition under Mild and Cocatalyst-Free Conditions.

CO2 is considered as the primary greenhouse gas, resulting in a series of serious environmental problems that affect people's life and health. Carbon capture and sequestration has been implemented as one of the most appealing pathways to control and use CO2 . Here, we rationally integrate various functional sites within the confined nanospace of a microporous metal-organic framework (MOF) material, which is constructed by mixed-ligand strategy based on metal-adeninate vertices. It not only exhibits excellent stability but also can efficiently transform CO2 and epoxides to cyclic carbonates under mild and cocatalyst-free conditions. Additionally, this catalyst shows extraordinary recyclability for the CO2 cycloaddition reaction.

Encapsulation of an Ionic Metalloporphyrin into a Zeolite Imidazolate Framework in situ for CO2 Chemical Transformation via Host-Guest Synergistic Catalysis.

It is a great challenge to rationally integrate multiple reactive sites into a composite material with confined nanospace, which can be applied as a nanoreactor to facilitate targeting catalytic reaction. In this work, an ionic metalloporphyrin has been encapsulated in situ into ZIF-8 for a solvent-free synthesis of cyclic carbonates from CO2 and epoxides without any co-catalyst under 1 atm CO2 .