Spatial transcriptomics analysis of esophageal squamous precancerous lesions and their progression to esophageal cancer.

Esophageal squamous precancerous lesions (ESPL) are the precursors of esophageal squamous cell carcinoma (ESCC) including low-grade and high-grade intraepithelial neoplasia. Due to the absence of molecular indicators, which ESPL will eventually develop into ESCC and thus should be treated is not well defined. Indicators, for predicting risks of ESCC at ESPL stages, are an urgent need. We perform spatial whole-transcriptome atlas analysis, which can eliminate other tissue interference by sequencing the specific ESPL regions. In this study, the expression of TAGLN2 significantly increases, while CRNN expression level decreases along the progression of ESCC. Additionally, TAGLN2 protein level significantly increases in paired after-progression tissues compared with before-progression samples, while CRNN expression decreases. Functional studies suggest that TAGLN2 promotes ESCC progression, while CRNN inhibits it by regulating cell proliferation. Taken together, TAGLN2 and CRNN are suggested as candidate indicators for the risk of ESCC at ESPL stages.

Toosendanin targeting eEF2 impedes Topoisomerase I & II protein translation to suppress esophageal squamous cell carcinoma growth.

BACKGROUND: Although molecular targets such as HER2, TP53 and PIK3CA have been widely studied in esophageal cancer, few of them were successfully applied for clinical treatment. Therefore, it is urgent to discover novel actionable targets and inhibitors. Eukaryotic translational elongation factor 2 (eEF2) is reported to be highly expressed in various cancers. However, its contribution to the maintenance and progression of cancer has not been fully clarified. METHODS: In the present study, we utilized tissue array to evaluate eEF2 protein expression and clinical significance in esophageal squamous cell carcinoma (ESCC). Next, we performed knockdown, overexpression, RNA-binding protein immunoprecipitation (RIP) sequence, and nascent protein synthesis assays to explore the molecular function of eEF2. Furthermore, we utilized compound screening, Surface Plasmon Resonance (SPR), Isothermal Titration Calorimetry (ITC) assay, cell proliferation and Patient derived xenograft (PDX) mouse model assays to discover an eEF2 inhibitor and assess its effects on ESCC growth. RESULTS: We found that eEF2 were highly expressed in ESCC and negatively associated with the prognosis of ESCC patients. Knocking down of eEF2 suppressed the cell proliferation and colony formation of ESCC. eEF2 bond with the mRNA of Topoisomerase II (TOP1) and Topoisomerase II (TOP2) and enhanced the protein biosynthesis of TOP1 and TOP2. We also identified Toosendanin was a novel inhibitor of eEF2 and Toosendanin inhibited the growth of ESCC in vitro and in vivo. CONCLUSIONS: Our findings show that Toosendanin treatment suppresses ESCC growth through targeting eEF2 and regulating downstream TOP1 and TOP2 biosynthesis. eEF2 could be supplied as a potential therapeutic target in the further clinical studies.

Erianin suppresses constitutive activation of MAPK signaling pathway by inhibition of CRAF and MEK1/2.

Constitutive activation of RAS-RAF-MEK-ERK signaling pathway (MAPK pathway) frequently occurs in many cancers harboring RAS or RAF oncogenic mutations. Because of the paradoxical activation induced by a single use of BRAF or MEK inhibitors, dual-target RAF and MEK treatment is thought to be a promising strategy. In this work, we evaluated erianin is a novel inhibitor of CRAF and MEK1/2 kinases, thus suppressing constitutive activation of the MAPK signaling pathway induced by BRAF V600E or RAS mutations. KinaseProfiler enzyme profiling, surface plasmon resonance (SPR), isothermal titration calorimetry (ITC), cellular thermal shift assay, computational docking, and molecular dynamics simulations were utilized to screen and identify erianin binding to CRAF and MEK1/2. Kinase assay, luminescent ADP detection assay, and enzyme kinetics assay were investigated to identify the efficiency of erianin in CRAF and MEK1/2 kinase activity. Notably, erianin suppressed BRAF V600E or RAS mutant melanoma and colorectal cancer cell by inhibiting MEK1/2 and CRAF but not BRAF kinase activity. Moreover, erianin attenuated melanoma and colorectal cancer in vivo. Overall, we provide a promising leading compound for BRAF V600E or RAS mutant melanoma and colorectal cancer through dual targeting of CRAF and MEK1/2.

3,3'-Diindolylmethane plus Eflornithine suppress DNA Replication and Cell Cycle in Esophageal Squamous Cell Carcinoma in vivo.

Esophageal squamous cell carcinoma (ESCC) is a malignant cancer that is responsible for a high mortality rate; it accounts for approximately 90% of the 456,000 esophageal cancer (EC) cases diagnosed annually. Effective natural or synthesized compounds to prevent, treat, and/or inhibit ESCC relapse are desperately needed. The natural di-indole compound 3,3'-diindolylmethane (DIM) is abundant in cruciferous vegetables and shows potent anti-tumor effects in multiple cancers. The synthesized Eflornithine (DFMO) is clinically used to treat African sleeping sickness. We demonstrated that the combination of DIM+DFMO could significantly suppress the ESCC growth in the in vivo study of three patient-derived xenograft (PDX) cases. Then, the corresponding underlying anticancer mechanisms were investigated via the isobaric tags for relative and absolute quantification (iTRAQ) on the proteome level. We found that the DNA Replication and Cell Cycle were the top-2 most significantly downregulated signaling pathways following the DIM+DFMO treatment. Correspondingly and interestingly, these two pathways were the top-2 upregulated ones in clinic ESCC tumors. Moreover, the involved differentially expressed genes (DEGs) including MCM2, MCM3, MCM5, MCM6, MCM7, CDK1, and LIG1 were all inversely downregulated by DIM+DFMO treatment. In the limited clinical study in two ESCC cases, the administration of DIM (250mg) +DFMO (500 mg) once daily showed favorable results, including alleviated swallowing difficulties, decreased blood tumor markers (CA19-9, CA15-3 and AFP), and no severe toxicity in at least one month progression free survival period. We concluded that DIM+DFMO is a promising therapeutic combination for ESCC treatment via the suppression of DNA Replication and Cell Cycle activities. However, these therapeutic effects should be verified in large cohort clinical trials with sufficient cases.

Soil texture is an important factor determining how microplastics affect soil hydraulic characteristics.

Microplastic pollution and changes to soil hydraulic characteristics affect the physical properties and functions of soil; however, knowledge remains limited on how microplastics influence soil hydraulic properties. Nonetheless, it is important to understand these relationships to maintain soil health and ensure sustainable land use, especially in the current "plastic age." This case study explored how different particle sizes (20, 200, and 500 µm) and concentrations (up to 6%) of polypropylene microplastics affect the hydraulic properties of three soil textures (loam, clay, and sand). The results show that addition of microplastic reduced the saturated hydraulic conductivity (Ks) of the three soils by 69.79%, 77.11%, and 95.79%, respectively. These observed adverse effects of microplastics on the infiltration properties of the three studied soils were influenced by particle size, with larger particles having the weakest effect. Furthermore, microplastic addition reduced the water retention capacity of the clay to a greater extent than that of the loam and sand. In the case of clay, the slope of the water characteristic curve (SWRC) increased significantly, whereas the saturated water content (θs) and residual water content (θr) curves decreased significantly. Importantly, the interaction between microplastics and soil alters the soil pore-size distribution and reduces pore availability. Overall, this case study demonstrates the impact of microplastic on the hydraulic properties of different soil textures, which can inform management strategies to minimize the adverse effects of microplastic accumulation on yields where plastics are used in agricultural production.

Fertility and early embryonic development toxicity and toxicokinetic study of KFP-H008 in Sprague-Dawley rats.

The novel potassium competitive acid blocker, KFP-H008, developed to overcome the shortcomings of proton pump inhibitors. In this study, KFP-H008 was administered by oral gavage at doses of 0 (control), 15, 45, and 150 mg/kg to Sprague-Dawley rats (24 animals per sex per group). Body weight, food consumption, mortality, sexual cycle, mating behavior, pregnancy, sperm motility, and relative organ weights were evaluated. In a concomitant toxicokinetic (TK) study (10 animals per sex per group), plasma TK parameters and tissue distribution of KFP-H008 were tested. There were obvious effects at the dosage of 150 mg/kg to male rats with decreases of prostate weight and lower weight gain; to female rats with lower weight gain, hair off, and lower corpus luteum count. There were no effects on litter parameters. Time to reach maximum plasma concentrations for KFP-H008 was between 0.5 and 1.0 hr for the 15 and 45 mg/kg groups, while for the 150 mg/kg group it had a delay to 2 hr. Overall, the NOAEL of KFP-H008 was considered to be 45 mg/kg in both genders and the TK study shows that exposure (area under the curve) of male rats was about 1,091.0 ± 530.8 µg/Lhr and to female rats was 1,030.5 ± 512.5 µg/Lhr. Administration of KFP-H008although reaches the reproductive organs, it demonstrated no significant effects on reproductive organs, it did not affect mating, fertility, pregnancy, growth, or morphologic development.

Two new calix[4]resorcinarene-based coordination cages adjusted by metal ions for the Knoevenagel condensation reaction.

Two new calix[4]resorcinarene-based coordination cages, namely, [Zn4(TPC4R)(PDC)4]·2DMF·6H2O (1-Zn) and [In11(TPC4R)2(PDC)16(µ2-OH)2(H2O)2]·[(CH3)2NH2]·8DMF·20H2O·EtOH (2-In), have been synthesized via solvothermal reactions (TPC4R = tetra(2-(4H-pyrazol-3-yl)pyridine)calix[4]resorcinarene, H2PDC = 3,5-pyridinedicarboxylic acid, DMF = N,N'-dimethylformamide). By carefully tuning different metal ions, two structurally different cages 1-Zn and 2-In were achieved. The former shows a bowl-shaped structure, while the latter features a dumbbell-like structure. After activation, they exhibited unsaturated Zn(ii) or In(iii) Lewis acid sites and the free nitrogen Lewis base sites of the PDC2-. Therefore, they were employed as catalysts for the Knoevenagel condensation reaction in the absence of a solvent. Particularly, 1-Zn featured high structural stability and enhanced the catalytic activity.

Proteomics Reveal the Inhibitory Mechanism of Levodopa Against Esophageal Squamous Cell Carcinoma.

High recurrence rates and poor survival of patients with esophageal squamous cell carcinoma (ESCC) after treatment make ongoing research on chemoprevention drugs for ESCC particularly important. In this study, we screened a large number of FDA-approved drugs and found levodopa, a drug used to treat Parkinson's disease, had an inhibitory effect on the growth of ESCC cells. To elucidate the molecular mechanisms involved, we applied quantitative proteomics to investigate the anti-tumor activity of levodopa on ESCC. The results suggest that levodopa could down-regulate oxidative phosphorylation, non-alcoholic fatty liver disease, and Parkinson's disease pathways. Major mitochondrial respiratory compounds were involved in the pathways, including succinate dehydrogenase subunit D, NADH-ubiquinone oxidoreductase Fe-S protein 4, and mitochondrial cytochrome c oxidase subunit 3. Down-regulation of these proteins was associated with mitochondrial dysfunction. Western blotting and immunofluorescence results confirmed the proteomics findings. Cell viability assays indicated mitochondrial activity was suppressed after levodopa treatment. Reduced mitochondrial membrane potential was detected using JC-1 staining and TMRE assays. Transmission electron microscopy revealed changes in the morphology of mitochondria. Taken together, these results indicate that levodopa inhibited the growth of ESCC through restraining mitochondria function.

Combination and distribution characteristics of syndromes related to traditional Chinese medicine in patients with chronic heart failure: Protocol for a clinical study.

INTRODUCTION: Chronic heart failure has become one of the main diseases endangering human health in the 21st century. It is characterized by high morbidity and high mortality. With the continuous in-depth study of Traditional Chinese medicine, the treatment of heart failure by Tradional Chinese medicine has made significant progress, especially in improving the clinical symptoms of patients, controlling the development of the disease, and improving the quality of life of patients. METHODS/DESIGN: This will be a retrospective, single-blind clinical observational study. All participants will receive chronic heart failure routine treatment and care. The researcher will fill in the case information collection form and collect multiple clinical diagnosis and treatment information. DISCUSSION: At present, there is very little research on the elements of chronic heart failure syndrome, and more exploration and excavation in this area are needed. So we designed this program. We aim to explore the distribution characteristics of Traditional Chinese medicine syndrome elements and combinations of chronic heart failure patients, and analyze the relationship between syndrome elements and related influencing factors. TRIAL REGISTRATION: ClinicalTrials.gov,ChiCTR2000034555, Registered on 18 May 2020.

Distribution of traditional Chinese medicine syndromes in type 2 diabetes mellitus with chronic heart failure: A clinical study.

INTRODUCTION: The incidence of type 2 diabetes has been increasing year by year in recent years. Type 2 diabetes is an important risk factor in the occurrence and development of heart failure, and it is the second potential risk factor after coronary artery disease. At present, there is no unified etiology, pathogenesis, and syndrome differentiation criteria for type 2 diabetes with chronic heart failure, and it is susceptible to subjective factors. Therefore, standardized, objective, and standardized research is needed to provide reference and guidance for clinical diagnosis and treatment. In this study, the theory of syndrome differentiation is used to initially explore the distribution of traditional Chinese medicine syndromes in patients with type 2 diabetes and chronic heart failure through case data collection, syndrome extraction, and clinical data analysis. METHODS/DESIGN: In this study, we will collect at least 500 cases of type 2 diabetes with chronic heart failure that meet the standard outpatient and hospitalization, and fill out the case information collection form. Then we will collect a number of clinical diagnosis and treatment information, and judge the syndrome based on the sum of the contribution of each syndrome to the relevant syndrome. We will use Microsoft Excel to establish a database, enter the relevant diagnosis and treatment, and syndrome information of the case information collection table, and verify and correct in time to ensure the accuracy of the data. DISCUSSION: This study will provide reference and guidance for the clinical diagnosis and treatment of type 2 diabetes with chronic heart failure. TRIAL REGISTRATION: ClinicalTrials.gov, ChiCTR2000033010, Registered on May 18, 2020.

Mefloquine Inhibits Esophageal Squamous Cell Carcinoma Tumor Growth by Inducing Mitochondrial Autophagy.

Esophageal squamous cell carcinoma (ESCC) has a worldwide impact on human health, due to its high incidence and mortality. Therefore, identifying compounds to increase patients' survival rate is urgently needed. Mefloquine (MQ) is an FDA-approved anti-malarial drug, which has been reported to inhibit cellular proliferation in several cancers. However, the anti-tumor activities of the drug have not yet been completely defined. In this study, mass spectrometry was employed to profile proteome changes in ESCC cells after MQ treatment. Sub-cellular localization and gene ontology term enrichment analysis suggested that MQ treatment mainly affect mitochondria. The KEGG pathway enrichment map of down-regulated pathways and Venn diagram indicated that all of the top five down regulated signaling pathways contain four key mitochondrial proteins (succinate dehydrogenase complex subunit C (SDHC), succinate dehydrogenase complex subunit D, mitochondrially encoded cytochrome c oxidase III and NADH: ubiquinone oxidoreductase subunit V3). Meanwhile, mitochondrial autophagy was observed in MQ-treated KYSE150 cells. More importantly, patient-derived xenograft mouse models of ESCC with SDHC high expression were more sensitive to MQ treatment than low SDHC-expressing xenografts. Taken together, mefloquine inhibits ESCC tumor growth by inducing mitochondrial autophagy and SDHC plays a vital role in MQ-induced anti-tumor effect on ESCC.

2,6-DMBQ is a novel mTOR inhibitor that reduces gastric cancer growth in vitro and in vivo.

BACKGROUND: Fermented wheat germ extract has been reported to exert various pharmacological activities, including anti-oxidant, anti-cell growth and cell apoptosis in various cancer cells. Although 2,6-dimethoxy-1,4-benzoquinone (2,6-DMBQ) is a benzoquinone compound and found in fermented wheat germ extract, its anticancer effects and molecular mechanism(s) against gastric cancer have not been investigated. METHODS: Anticancer effects of 2,6-DMBQ were determined by MTT, soft agar, cell cycle and Annexin V analysis. Potential candidate proteins were screened via in vitro kinase assay and Western blotting. mTOR knockdown cell lines were established by lentiviral infection with shmTOR. The effect of 2,6-DMBQ on tumor growth was assessed using gastric cancer patient-derived xenograft models. RESULTS: 2,6-DMBQ significantly reduced cell growth and induced G1 phase cell cycle arrest and apoptosis in gastric cancer cells. 2,6-DMBQ reduced the activity of mTOR in vitro. The inhibition of cell growth by 2,6-DMBQ is dependent upon the expression of the mTOR protein. Remarkably, 2,6-DMBQ strongly reduced patient-derived xenograft gastric tumor growth in an in vivo mouse model. CONCLUSIONS: 2,6-DMBQ is an mTOR inhibitor that can be useful for treating gastric cancer. It has therapeutic implications for gastric cancer patients.

Wavelength-tunable bidirectional passively Q-switched Er-doped fiber laser incorporating a single-walled carbon nanotube and tunable bandpass filter.

We demonstrated a continuously wavelength-tunable bidirectional passively $ Q $Q-switched fiber laser based on a single-walled carbon nanotube saturable absorber and a bandpass filter (BPF). By tuning the commercial BPF, the $ Q $Q-switched pulse can be obtained in the same cavity at the same pump power in clockwise (CW) and counter-clockwise (CCW) directions. The central wavelength can be continuously tuned from 1520.88 to 1568.56 nm in the CW direction, and from 1520.96 to 1568.64 nm in the CCW direction. A wide tuning range of 48 nm is achieved for two directions in the passively $ Q $Q-switched fiber laser. During the tuning process of the fiber laser, the output pulses with the same central lasing wavelength can be obtained in both oscillation directions owing to the BPF. By increasing the pump power from 130 to 350 mW, the cavity delivers a $ Q $Q-switched pulse with the central wavelength of 1560 nm whose repetition rate changes from 9.64 to 59.18 kHz for the CW direction. In the CCW direction, the repetition rate of the $ Q $Q-switched pulse changes from 10.26 to 61.03 kHz. To the best of our knowledge, it is the first time that continuous wavelength-tunable passively $ Q $Q-switched pulses have been achieved in a bidirectional erbium-doped fiber laser.

CELF2 suppresses non-small cell lung carcinoma growth by inhibiting the PREX2-PTEN interaction.

The phosphoinositide 3-kinase (PI3-K)/Akt signaling pathway is important in the regulation of cell proliferation through its production of phosphatidylinositol 3,4,5-triphosphate (PIP3). Activation of this pathway is frequently observed in human cancers, including non-small cell lung carcinoma. The PI3-K/Akt pathway is negatively regulated by the dual-specificity phosphatase and tensin homolog (PTEN) protein. PTEN acts as a direct antagonist of PI3-K by dephosphorylating PIP3. Studies have shown that PTEN phosphatase activity is inhibited by PREX2, a guanine nucleotide exchanger factor (GEF). Multiple studies revealed that CELF2, an RNA binding protein, cooperates synergistically with PTEN as a tumor suppressor in multiple cancers. However, the underlying mechanism as to how CELF2 enhances PTEN activity remains unclear. Here, we report that CELF2 interacts with PREX2 and reduces the association of PREX2 with PTEN. Consistent with this observation, PTEN phosphatase activity is upregulated with CELF2 overexpression. In addition, overexpression of CELF2 represses both Akt phosphorylation and cell proliferation only in the presence of PTEN. In an ex vivo study, CELF2 gene delivery could significantly inhibit patient-derived xenografts (PDX) tumor growth. To further investigate the clinical relevance of this finding, we analyzed 87 paired clinical lung adenocarcinoma samples and the results showed that CELF2 protein expression is downregulated in tumor tissues and associated with poor prognosis. The CELF2 gene is located on the chromosome 10p arm, a region frequently lost in human cancers, including breast invasive carcinoma, low-grade glioma and glioblastoma. Analysis of TCGA datasets showed that CELF2 expression is also associated with shorter patient survival time in all these cancers. Overall, our work suggests that CELF2 plays a novel role in PI3-K signaling by antagonizing the oncogenic effect of PREX2.

Water-Stable Metal-Organic Framework for Effective and Selective Cr2O72- Capture through Single-Crystal to Single-Crystal Anion Exchange.

Effective and selective capture of environmentally toxic Cr2O72- from water is desirable for both environment protection and human health, but it still remains a significant challenge. We present a water-stable cationic metal-organic framework (MOF) with large nanotubular channels ( ca. 1.4 × 1.4 nm2), (1-Cl). Remarkably, the resulting porous material exhibits rapid aqueous-phase removal of Cr2O72- via an anion-exchange manner. Meaningfully, the capture and separation of aqueous Cr2O72- are highly selective even in the presence of other disturbing anions. More importantly, the crystal structure of 1-Cl after anion exchange (1-Cr2O7) could be determined by single crystal X-ray diffraction, elaborating the single-crystal-to-single-crystal (SC-SC) transformation. The Cr2O72- removal process by 1-Cl thus was directly uncovered by the crystal structure of Cr2O72--incorporated 1-Cr2O7.

Losmapimod Overcomes Gefitinib Resistance in Non-small Cell Lung Cancer by Preventing Tetraploidization.

The epidermal growth factor receptor (EGFR) is known to play a critical role in non-small cell lung cancer (NSCLC). Constitutively active EGFR mutations, including in-frame deletion in exon 19 and L858R point mutation in exon 21, contribute about 90% of all EGFR-activating mutations in NSCLC. Although oral EGFR-tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib, show dramatic clinical efficacy with significantly prolonged progression-free survival in patients harboring these EGFR-activating mutations, most of these patients will eventually develop acquired resistance. Researchers have recently named genomic instability as one of the hallmarks of cancer. Genomic instability usually involves a transient phase of polyploidization, in particular tetraploidization. Tetraploid cells can undergo asymmetric cell division or chromosome loss, leading to tumor heterogeneity and multidrug resistance. Therefore, identification of signaling pathways involved in tetraploidization is crucial in overcoming drug resistance. In our present study, we found that gefitinib could activate YAP-MKK3/6-p38 MAPK-STAT3 signaling and induce tetraploidization in gefitinib-resistance cells. Using p38 MAPK inhibitors, SB203580 and losmapimod, we could eliminate gefitinib-induced tetraploidization and overcome gefitinib-resistance. In addition, shRNA approach to knockdown p38α MAPK could prevent tetraploidy formation and showed significant inhibition of cancer cell growth. Finally, in an in vivo study, losmapimod could successfully overcome gefitinib resistance using an in-house established patient-derived xenograft (PDX) mouse model. Overall, these findings suggest that losmapimod could be a potential clinical agent to overcome gefitinib resistance in NSCLC.

Highly Stable Copper(I)-Based Metal-Organic Framework Assembled with Resorcin[4]arene and Polyoxometalate for Efficient Heterogeneous Catalysis of Azide-Alkyne "Click" Reaction.

A new highly stable copper(I)-based metal-organic framework (MOF), namely, [CuI4(SiW12O40)(L)]·6H2O·2DMF (1), was synthesized by incorporating Keggin-type polyoxometalate (POM) anions and a functionalized wheel-like resorcin[4]arene-based ligand (L) under sovothermal condition. 1 exhibits a charming 3D supramolecular architecture sandwiched by the POM anions. Noticeably, 1 has exceptional chemical stability, especially in organic solvents or aqueous solutions with a wide range of pH values. Considering the catalytically active Cu(I) sites in 1, the azide-alkyne cycloaddition (AAC) reaction was studied by employing 1 as the heterogeneous catalyst. Most strikingly, 1 exhibits excellent catalytic activity as well as recyclability for the AAC reaction.

Resorcin[4]arene-Based Microporous Metal-Organic Framework as an Efficient Catalyst for CO2 Cycloaddition with Epoxides and Highly Selective Luminescent Sensing of Cr2O72.

A stable microporous anionic metal-organic framework (MOF), [(CH3)2NH2]6[Cd3L(H2O)2]·12H2O (1), has been synthesized via solvothermal assembly of a new resorcin[4]arene-functionalized dodecacarboxylic acid (H12L) and Cd(II) cations. The constructed MOF (1) was characterized by single-crystal X-ray diffraction and other physicochemical analyses. 1 exhibits a fascinating 3D microporous framework structure, in which the free water molecules and the [(CH3)2NH2]+ cations were located. Remarkably, the exposed Lewis acid Cd(II) sites of activated 1 make it an efficient heterogeneous catalyst for the cycloaddition of CO2 with epoxides at 1 and 20 atm. Importantly, the activated samples of 1 can be reused at least five circles with excellent catalytic performance. Moreover, the fluorescence detection of Cr2O72- and Fe3+ was studied by using 1 as a potential luminescent sensor.

A Polyoxovanadate-Resorcin[4]arene-Based Porous Metal-Organic Framework as an Efficient Multifunctional Catalyst for the Cycloaddition of CO2 with Epoxides and the Selective Oxidation of Sulfides.

In this work, we report a new polyoxovanadate-resorcin[4]arene-based metal-organic framework (PMOF), [Co2L0.5V4O12]·3DMF·5H2O (1), assembled with a newly functionalized wheel-like resorcin[4]arene ligand (L). 1 features an elegant porous motif and represents a rare example of PMOFs composed of both a resorcin[4]arene ligand and polyoxovanadate. Remarkably, 1 shows open V sites in the channel, which makes 1 an efficient heterogeneous Lewis acid catalyst for the cycloaddition of carbon dioxide to epoxides with high conversion and selectivity. Strikingly, 1 also exhibits high catalytic activity for the heterogeneous oxidative desulfurization of sulfides. Particularly, the heterogeneous catalyst 1 can be easily separated and reused with good catalytic activity.

Value of ultrasonography for observation of early healing of humeral shaft fractures.

PURPOSE: Explore the value of ultrasonography for observation of early healing of humeral shaft fractures. METHODS: Sixty-five humeral shaft fracture patients were recruited. They were examined sonographically with color Doppler ultrasonography (CDU) and/or power Doppler ultrasonography (PDU) during the 1st week, 2nd week, 3rd week, 4th week, 9th week, and 15th week after the initial surgical procedure of internal fixation. Formation of callus consolidation and the resistance indexes (RI) of blood flow in different durations were compared between the good healing group and bad healing (delayed fracture healing or nonunion) group. RESULTS: Ultrasound showed that 59 patients had good fracture healing. Within the 2nd and 4th week after surgery, the RI decreased over time (P < 0.05) and color Doppler flow imaging (CDFI/PDU) grading ranged from II to III. Six patients had bad fracture healing (delayed healing or nonunion). Insufficient or absent blood flow signals demonstrated that no callus was found in and/or around the fracture sites. CDFI grading ranged from 0 to I. There was significant difference compared with the good healing group (P < 0.05). CONCLUSION: CDFI/PDU is an easy, painless, and effective method for predicting the prognosis of humeral shaft fractures by estimating early healing.