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C40H42O14N8Cl4Cd, triclinic, P1̄ (no. 2), a = 7.5892(16) Å, b = 7.6583(15) Å, c = 20.629(4) Å, α = 79.620(4)°, β = 84.594(3)°, γ = 79.427(4)°, V = 1157.0(4) Å3, Z = 1, R gt(F) = 0.0721, wR ref(F 2) = 0.1967, T = 296(2) K.

C60H68O4N12Cl10Mn, triclinic, P1‾$P\overline{1}$ (no. 2), a = 8.9262(11) Å, b = 13.7013(18) Å, c = 15.330(2) Å, α = 91.414(2)°, β = 98.951(2)°, γ = 106.688(2)°, V = 1769.3(4) Å3, Z = 1, Rgt(F) = 0.0443, wRref(F2) = 0.1222, T = 296(2) K.

C60H68O4N12Br2Cl8Zn, triclinic, P 1‾ $\overline{1}$ (no. 2), a = 9.0149 (13) Å, b = 13.671 (2) Å, c = 15.168 (2) Å, α = 92.280 (3)°, β = 97.441 (2)°, γ = 107.862 (2)°, V = 1758.0 (4) A3, Z = 1, R gt (F) = 0.0417, wR ref (F 2) = 0.1005, T = 296 (2) K.

C60H68O4N12Cl10Zn, triclinic, P 1‾ $\overline{1}$ (no. 2), a = 8.816 (2) Å, b = 13.688 (4) Å, c = 15.169 (4) Å, α = 91.085 (5)°, β = 98.609 (4)°, γ = 106.874 (5)°, V = 1728.2 (8) A3, Z = 1, Rgt (F) = 0.0615, wR ref(F 2) = 0.1709, T = 296 (2) K.

Glycerylphosphorylcholine (GPC) was prepared by transesterification using supported sodium methoxide as catalyst and natural lecithin as raw material. Sodium methoxide has been proved to be an effective catalyst for the preparation of GPC, which is easy to recover and reuse. After six repeated uses, its stability is satisfactory. The effects of agitation speed, catalyst dosage, and reaction temperature on the reaction were investigated, respectively, and the optimum conditions for preparing GPC catalyzed by supported sodium methoxide were found: the concentration of phosphorylcholine was 0.1 mol·L−1, the stirring speed was 600 rpm, the amount of catalyst was 7.5 g·L−1, the reaction temperature was 45°C, and the reaction time was 4 h; then, the conversion rate of phosphatidylcholine could reach 99%. At the same time, the reaction kinetic model was established based on the mechanism of the transesterification, and the experimental data were compared with the calculated values; it was found that the experimental data fitted the model well. Finally, the reaction activation energy obtained by the Arrhenius equation is 41.6 kJ·mol−1, which indicates that the supported sodium methoxide has good catalytic performance in this reaction system.

C8H11N8O6, monoclinic, P21/n (no. 14), a = 5.6348(8) Å, b = 19.485(3) Å, c = 11.5316(17) Å, β = 101.013(2)°, V = 1242.8(3) Å3, Z = 4, Rgt(F) = 0.0396, wRref(F2) = 0.1039, T = 296(2) K.

Abstract Background With the expanded utilization of transcatheter aortic valve implantation (TAVI) to younger and lower surgical risk patients with severe aortic stenosis (AS), optimal medical therapy after TAVI procedure has become the main concern. Renin-angiotensin system inhibitors (RASi) are widely utilized in the area of cardiovascular disease including heart failure and myocardial infarction and revealed the ability to reverse left ventricular (LV) remodeling. Interests have, thus, been drawn in investigating whether the prescription of RASi after the TAVI procedure can prevent or reverse cardiac remodeling and improve long-term clinical outcomes. No recommendation regarding the prescription of RASi after TAVI is proposed yet due to the lack of evidence from randomized controlled trials, especially in the Chinese population. We, therefore, designed this randomized controlled trial to explore the effect of adding fosinopril to standard care in patients who underwent a successful TAVI procedure on the LV remodeling. Methods A total of 200 post-TAVI patients from seven academic hospitals across China will be recruited and randomized with a ratio of 1:1 to receive standard care or standard care plus fosinopril. Follow-up visits will take place at 30 days, 3 months, 6 months, 12 months, and 24 months from randomization to assess the clinical symptoms, any adverse events, cardiac function, and quality of life. Cardiac magnetic resonance will be performed at baseline and repeated at the 24-month follow-up visit to assess LV remodeling. Discussion This study will provide evidence regarding medical therapy for AS patients who underwent TAVI and filling the gap in the Chinese population. Trial registration Chinese Clinical Trial Registry ChiCTR2100042266 . Registered on 17 January 2021

Pericytes play important roles in retinal vascular mature and homeostasis. Their dysfunction is apathological manifestation in diabetes retinopathy. Circular RNAs have emerged as a class of regulatory RNA tran‐scripts and are involved in the regulation of several physiological and pathological processes. In this study, diabe‐tes-related stresses led to increased expression of circ_0001186 in pericytes but had no effects on the expression ofcirc_0001186 in endothelial cells. In vitro studies showed that circ_0001186 knockdown reduced high glucose-in‐duced pericyte injury, contributed to the proliferation of pericytes and the recruitment of pericytes to endothelialcells. In vivo studies showed that conditional knockdown of circ_0001186 in pericytes decreased diabetes-inducedpericyte loss, suppressed retinal vascular leak and inflammatory response. Mechanistically, knockdown of circ_0001186 could activate PDGF-PI3K-Akt signaling and protect pericytes against high glucose-induced injury. Thisstudy revealed a novel mechanism of retinal vascular dysfunction. Targeting of pericyte-expressed circ_0001186provides a novel insight into the treatment of diabetes retinopathy.

The adsorption of l-α-glycerophosphocholine (GPC) by cation-exchange resin 001 × 7 was studied in a batch system. The adsorbent dosage, shaking speed, and adsorption temperature were investigated. An adsorption efficiency of more than 99.4% was obtained under optimal conditions. The kinetic data evaluated by the pseudo-second-order kinetic model fitted the experimental data better than those evaluated by the pseudo-first-order model. The rate constant k2 increased when the temperature increased, indicating the adsorption was endothermic in nature. The Langmuir and Freundlich isotherm models were used to analyze the adsorption equilibrium data, and it was found that the experimental data well fitted the Langmuir isotherm model. The thermodynamic parameters, enthalpy change (ΔG0), free energy change (ΔH0), and entropy change (ΔS0), were calculated. The value of ΔG0 was found to be in the range of −5.09 to −14.20 kJ mol−1, indicating that the adsorption was spontaneous and basically physisorption, and the positive values of ΔH0 and ΔS0 exhibited that the adsorption was endothermic and the randomness of the system increased during the adsorption.

C5H10N8O4S, Orthorhombic, Pba2 (no. 32), a = 7.7320(11) Å, b = 12.8686(19) Å, c = 5.0657(8) Å, β = 90°, V = 504.04(13) Å3, Z = 2, R gt(F) = 0.0298, wR ref(F 2) = 0.0748, T = 296(2) K.

Abstract Background Knee osteoarthritis (KOA) is characterized by mitochondrial damage and increased inflammation. Circulating cell-free mitochondrial DNA (ccf-mtDNA), which originates from damaged mitochondria, is an endogenous damage-associated molecular pattern (DAMPs) molecule that may trigger inflammation and is recognized as a potential biomarker for various diseases. In this study, we investigated the potential association between plasma ccf-mtDNA content and its use as a diagnostic biomarker in patients with KOA. Methods We collected plasma samples from patients with KOA and healthy controls (HC). Subsequently, quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect ccf-mtDNA content in the plasma samples. We used the Kellgren–Lawrence (K-L) classification criteria to classify patients with KOA into four grades: I-IV. Disease severity in patients with KOA was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Next, Spearman analysis was performed to observe the correlation between ccf-mtDNA content and the K-L classification and WOMAC score. Logistic regression analysis was used to evaluate the relationship between ccf-mtDNA and KOA risk. Results In total, we enrolled 60 patients with KOA and HC who were matched for age, sex, and body mass index (BMI). We found that plasma ccf-mtDNA contents were significantly higher in patients with KOA (median, 2.44; quartile range, 1.10–3.79) than in HC (median, 1.08; quartile range, 0.52–2.12) (P