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A new binuclear Zn(II) complex, [Zn2L2(BIPY)2(H2O)2](1) (H2L = homophthalic acid, BIPY = 2,2'-bipyridine) has been synthesized by one-pot method of homophthalic acid, 2,2'-bipyridine, zinc acetate dihydrate, and NaOH in water/ethanol (v:v = 1:1) solution. The structure of complex (1) was characterized by IR and X-ray single-crystal diffraction analysis. The results show that each Zn(II) ion is five-coordinated with two carboxylic O atoms from two homophthalate ligands (O2, O3 or O2a, O3a), two N atoms from two 2,2'-bipyridine ligands (N1, N2 or N1a, N2a) and one O atom from coordinated water molecule (O5 or O5a), and forms a distorted trigonal bipyramid coordination geometry. Complex (1) forms 1D chained structure and 3D network structure by the p-p interaction of 2,2'-bipyridine ligands. The Hirschfeld surface analysis of complex (1) was calculated. The catalytic performance of complex (1) has also been investigated for the oxidation of benzyl alcohol under O2 atmosphere. The optimal reaction temperature and pressure were 100 °C and 0.3 MPa for complex (1). Copyright © 2022 by Authors, Published by BCREC Group. This is an open access article under the CC BY-SA License (https://creativecommons.org/licenses/by-sa/4.0).

C39H49N7O9Br2ClEr, triclinic, P 1 ‾ $P\overline{1}$ (no. 2), a = 12.3164(9) Å, b = 12.7581(9) Å, c = 14.5023(11) Å, α = 70.873(2)°, β = 80.281(2)°, γ = 65.810(2)°, V = 1962.4(3) Å3, Z = 1, R gt (F) = 0.0383, wR ref (F 2) = 0.0765, T = 296.15 K.

C34H26N4O5Mn, monoclinic, C2/c (no. 15), a = 29.4330(18) Å, b = 10.4120(6) Å, c = 20.0207(12) Å, β = 107.246(6)°, V = 5859.6(6) Å3, Z = 8, R gt (F) = 0.0380, wR ref (F 2) = 0.0865, T = 200 K.

In ethanol-water (v:v = 1:1), a new Ni(II) complex, [Ni(L)2(H2O)2] (1) (HL = 6-phenylpyridine-2-carboxylic acid) was synthesized using 6-phenylpyridine-2-carboxylic acid, NaOH and Ni(CH3COO)2.4H2O. The structure of complex 1 has been determined by elemental analysis and single crystal X-ray diffraction. The single crystal analysis shows that complex 1 contains one Ni(II) ion, two L ligands and two coordinated water molecules. In 1, the Ni(II) ion is six-coordinated to two O atoms and two N atoms from L ligands and two O atoms from coordinated water molecules, respectively, which form a distorted octahedral coordination geometry. The whole unit of complex 1 is interconnected to each other through intermolecular N−H•••O hydrogen bonds involving oxygen atom of coordinated water molecule and the oxygen atoms of L ligand to form 1D molecular architecture. The catalytic activity of complex 1 for oxidation of benzyl alcohol with O2 was investigated. The complex 1 shows good catalytic performance for the oxidation of benzyl alcohol, the benzyl alcohol conversion, benzaldehyde selectivity, and benzaldehyde yield were 49.1%, 92.0%, and 45.2%, respectively, at 90 °C under 0.7 Mpa O2 for 2 h. Moreover, complex 1 could be recovered easily by centrifugation and used repetitively for at least four times. Copyright © 2022 by Authors, Published by BCREC Group. This is an open access article under the CC BY-SA License (https://creativecommons.org/licenses/by-sa/4.0).

Objective: PCSK9 (proprotein convertase subtilisin/kexin type 9) plays a critical role in cholesterol metabolism via the PCSK9–LDLR (low-density lipoprotein receptor) axis in the liver; however, evidence indicates that PCSK9 directly contributes to the pathogenesis of various diseases through mechanisms independent of its LDL-cholesterol regulation. The objective of this study was to determine how PCSK9 directly acts on vascular smooth muscle cells (SMCs), contributing to degenerative vascular disease. Approach and Results: We first examined the effects of PCSK9 on cultured human aortic SMCs. Overexpression of PCSK9 downregulated the expression of ApoER2 (apolipoprotein E receptor 2), a known target of PCSK9. Treatment with soluble recombinant human ApoER2 or the DNA synthesis inhibitor, hydroxyurea, inhibited PCSK9-induced polyploidization and other cellular responses of human SMCs. Treatment with antibodies against ApoER2 resulted in similar effects to those observed with PCSK9 overexpression. Inducible, SMC-specific knockout of Pcsk9 accelerated neointima formation in mouse carotid arteries and reduced age-related arterial stiffness. PCSK9 was expressed in SMCs of human atherosclerotic lesions and abundant in the “shoulder” regions of vulnerable atherosclerotic plaques. PCSK9 was also expressed in SMCs of abdominal aortic aneurysm, which was inversely related to the expression of smooth muscle α-actin. Conclusions: Our findings demonstrate that PCSK9 inhibits proliferation and induces polyploidization, senescence, and apoptosis, which may be relevant to various degenerative vascular diseases.

Background Previous studies reported the prognostic value of the atherogenic index of plasma (AIP) in the course of atherosclerosis and other cardiovascular diseases (CVDs). Still, the predictive utility of the AIP is unknown among patients with type 2 diabetes mellitus (T2DM). Methods This was a secondary analysis of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, which randomized 10,251 patients with long-lasting T2DM. ROC curve analysis was used to determine an optimal threshold for AIP, and the study population was divided into high and low AIP groups. Univariable and multivariable Cox proportional hazards regression analyses were used to determine the association between AIP and primary (major adverse cardiovascular events [MACEs], including nonfatal myocardial infarction, nonfatal stroke, and/or death from cardiovascular causes) and secondary outcomes (all-cause mortality). Stratified analyses were performed to control for the confounding factors. Results AIP was an independent risk factor for the prognosis of T2DM (HR = 1.309; 95% CI 1.084–1.581; P = 0.005). The threshold for AIP was determined to be 0.34 in the study population. After adjustments for confounding factors, multivariable analysis showed that AIP was associated with the risk of MACEs (Model 1: HR = 1.333, 95% CI 1.205–1.474, P P = 0.016; Model 3: HR = 1.194, 95% CI 1.049–1.360, P = 0.007), all-cause mortality (Model 1: HR = 1.184, 95% CI 1.077–1.303, P P P = 0.036), and nonfatal myocardial infarction (Model 1: HR = 1.447, 95% CI 1.255–1.669, P P = 0.015; Model 3: HR = 1.284, 95% CI 1.071–1.539, P = 0.007). Subgroup stratified analyses showed that AIP might interact with sex, a classical risk factor of cardiovascular events. Conclusions This study showed that AIP might be a strong biomarker that could be used to predict the risk of cardiovascular events in patients with T2DM. Trial registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00000620.

C27H31N3O9Mn, monoclinic, P21/n (no. 14), a = 10.8917(9) Å, b = 11.2673(16) Å, c = 23.077(3) Å, β = 93.319(10)°, V = 2827.2(6) Å3, Z = 4, R gt (F) = 0.0735, wR ref (F 2) = 0.1938, T = 250 K.

A new six coordinated tetra-nuclear macrocyclic Zn(II) complex, ZnL4(Phen)2 (1) (HL= 3-bromo-2-hydroxybenzaldehyde-pyridine-2-carbohydrazone, Phen = 1,10-phenanthroline) has been synthesized by the self-assembly of 3-bromo-2-hydroxybenzaldehyde-pyridine-2-carbohydrazone, Zn(CH3COO)2•2H2O, NaOH and 1,10-phenanthroline in water/ethanol (v:v = 1:3) solution. Complex 1 was characterized by elemental analysis, infra red (IR), and single-crystal X-ray diffraction (XRD) analysis. The results show that Zn1 and Zn1b ions are six-coordinated with a distorted octahedral geometric configuration by four O atoms of two different L ligands and two N atoms of two different L ligands, Zn1a and Zn1c ions are also six-coordinated with a distorted octahedral geometric configuration by two N atoms of two different L ligands, two N atoms of Phen ligands and two O atoms of two different L ligands. Complex (1) forms 3D network structure by the - interaction. The selective oxidation reactions of benzyl alcohols catalyzed by complex (1) was investigated. The highest benzyl alcohol conversion and benzaldehyde selectivity were obtained at 100 °C for 4 h under 5 bar of O2. Copyright © 2021 by Authors, Published by BCREC Group. This is an open access article under the CC BY-SA License (https://creativecommons.org/licenses/by-sa/4.0).

Aims: During the COVID-19 epidemic, chest computed tomography (CT) has been highly recommended for screening of patients with suspected COVID-19 because of an unclear contact history, overlapping clinical features, and an overwhelmed health system. However, there has not been a full comparison of CT for diagnosis of heart failure or COVID-19 pneumonia. Methods: Patients with heart failure ( n=23) or COVID-19 pneumonia ( n=23) and one patient with both diseases were retrospectively enrolled. Clinical information and chest CT images were obtained and analyzed. Results: There was no difference in ground-glass opacity, consolidation, crazy paving pattern, the lobes affected, and septal thickening between heart failure and COVID-19 pneumonia. However, a less rounded morphology (4% vs. 70%, P=0.00092), more peribronchovascular thickening (70% vs. 35%, P=0.018) and fissural thickening (43% vs. 4%, P=0.002), and less peripheral distribution (30% vs. 87%, P=0.00085) were found in the heart failure group than in the COVID-19 group. Importantly, there were also more patients with upper pulmonary vein enlargement (61% vs. 4%, P=0.00087), subpleural effusion (50% vs. 0%, P=0.00058), and cardiac enlargement (61% vs. 4%, P=0.00075) in the heart failure group than in the COVID-19 group. Besides, more fibrous lesions were found in the COVID-19 group, although there was no statistical difference (22% vs. 4%, P=0.080). Conclusions: Although there is some overlap of CT features between heart failure and COVID-19, CT is still a useful tool for differentiating COVID-19 pneumonia.

C27H31N3O9Co, monoclinic, P21/n (no. 14), a = 10.9230(6) Å, b = 11.1166(8) Å, c = 22.8312(15) Å, β = 93.404(6)°, V = 2767.4(3) Å3, Z = 4, R gt (F) = 0.0349, wR ref (F 2) = 0.0893, T = 200 K.

C36H26N4O5Ni, orthorhombic, P212121 (no. 19), a = 10.5860(9) Å, b = 10.6497(6) Å, c = 26.4492(15) Å, β = 90°, V = 2981.8(3) Å3, Z = 4, R gt (F) = 0.0341, wR ref (F 2) = 0.0703, T = 200 K.

C34H24N4O4Zn, monoclinic, I2/a (no. 15), a = 18.2546(14) Å, b = 11.0510(7) Å, c = 16.1874(15) Å, β = 119.605(11)°, V = 2839.2(5) Å3, Z = 4, R gt (F) = 0.0302, wR ref (F 2) = 0.0694, T = 200 K.

C10H14N3O5SNa, triclinic, P 1 ‾ $P\overline{1}$ (no. 2), a = 6.7015(5) Å, b = 7.5656(5) Å, c = 14.1332(8) Å, β = 93.159(5)°, V = 654.71(8) Å3, Z = 2, R gt (F) = 0.0357, wR ref (F 2) = 0.0872, T = 273 K.

C36H26N4O5Co, monoclinic, C2/c (no. 15), a = 29.3826(17) Å, b = 10.3153(5) Å, c = 19.9407(12) Å, β = 107.263(6), V = 5771.6(6) Å3, Z = 8, R gt (F) = 0.0341, wR ref (F 2) = 0.0777, T = 200 K.

Objective: Remnant cholesterol (remnant-C) predicts atherosclerotic cardiovascular disease, regardless of LDL cholesterol (LDL-C) levels. This study assessed the associations between remnant-C and cardiovascular outcomes in type 2 diabetes mellitus. Research design and methods: This post-hoc analysis of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial used patient (type 2 diabetes >3 months) remnant-C and major adverse cardiovascular event (MACE) data from the study database. The associations between remnant-C and MACEs were evaluated using Cox proportional hazards regression analyses. We examined the relative MACE risk in remnant-C versus LDL-C discordant/concordant groups using clinically relevant LDL-C targets by discordance analyses. Results: The baseline analysis included 10,196 participants, with further visit-to-visit variability analysis including 9650 participants. During follow-up (median, 8.8 years), 1815 (17.8%) patients developed MACEs. After adjusting for traditional cardiovascular risk factors, each 1-SD increase in remnant-C was associated with a 7% higher MACE risk (HR=1.07, 95% CI: 1.02-1.12; P=0.004). In the fully adjusted model, the visit-to-visit remnant-C variability calculated using logSD (HR=1.41, 95% CI: 1.18-1.69, P100 or ≤100 mg/dL), high baseline remnant-C was associated with a higher MACE risk (HR=1.37, 95% CI: 1.09-1.73; P=0.007; HR=1.22, 95% CI: 1.04-1.41; P=0.015, respectively). Conclusions: Remnant-C levels were associated with MACEs in type 2 diabetic patients independent of LDL-C, and visit-to-visit remnant-C variability helped identify those with higher cardiovascular risk.

A new Cu(II) complex, [CuL2(H2O)2]·H2O (HL = N-nicotinoylglycine), has been obtained using N-nicotinoylglycine, copper(II) acetate monohydrate and NaOH as raw materials. The structure of the Cu(II) complex was characterized by elemental analysis and single crystal X-ray diffraction analysis. The Cu(II) ion is six-coordinated with two N atoms from two pyridine groups of L ligand and four O atoms of four coordinated H2O molecules. The Cu(II) complex forms a 2D layered structure and 3D network structure by the interaction of O-H···O hydrogen bonds. The catalytic activities of the Cu(II) complex catalyst for benzyl alcohol oxidation were determined with molecular oxygen as oxidant.

Background Massive hemorrhagic ascites caused by endometriosis is exceedingly rare, and the treatment strategy remains controversial. Here, we report a case of endometriosis with massive hemorrhagic ascites treated with a novel triple therapy including conservative surgery, gonadotropin-releasing hormone agonist, and then dienogest. Case summary A 28-year-old nulliparous patient was admitted to Shengjing Hospital of China Medical University, and exploratory laparoscopy was performed. A total of 9500 mL of brown ascites was aspirated from the pelvic cavity, the bilateral ovaries strongly adhered to the posterior of the uterus and were fixed to the pelvic floor, and endometriotic cysts were not observed in either ovary. The pelvic and abdominal peritonea were covered with patchy red, white, and brown endometriotic lesions and defects. Partial surgical resection of endometriotic lesions on the peritoneum was performed while we simultaneously collected multiple peritoneal biopsies. The final pathological diagnosis was endometriosis coupled with hemorrhagic necrotic tissue. Conclusion Postoperative injection of gonadotropin-releasing hormone agonist was provided three times, followed by dienogest administration, and we will continue to follow up with this ongoing treatment.

Transcatheter closure (TCC) has emerged as the first-line treatment for coronary artery fistulas. However, limited data exist regarding the long-term outcomes and technical aspects of this procedure. We aimed to report the long-term outcomes and technical aspects of TCC of large coronary-cameral fistulas (CCFs).All patients with large CCFs who underwent attempted TCC using the patent ductus arteriosus (PDA) occluder or Amplatzer vascular plug (AVP), from June 2002 to December 2017, were retrospectively reviewed. A total of 23 patients with large CCFs underwent attempted TCC using the PDA occluder or AVP. Most CCFs originated from the right coronary artery and drained predominantly into the right heart chamber. Procedural success was achieved in 21 (91.3%) patients. Devices were deployed using the arteriovenous loop in 15, transarterial approach in 4, and arterio-artery loop approach in 2 patients. Procedural complications included coronary spasm in one and side branch occlusion in one patient. Among these 21 patients with successful device implantation, follow-up angiograms or computed tomography angiograms were obtained in 14 (66.7%) patients at a median of 11.0 (range, 9.8-16.3) months. Late complications included thrombosis of residual fistula segment without myocardial infarction (MI) in one, coronary thrombosis resulting in MI in one, and recanalization necessitating re-intervention in one patient. No death and device embolization occurred.TCC of large CCFs using the PDA occluder or AVP is an effective therapy in anatomically suitable candidates, with favorable long-term outcomes. Given that potentially hazardous complications may occur late after the procedure, long-term periodic evaluation is mandatory.

Proprotein convertase subtilisin/kexin type-9 (PCSK9), a member of the proprotein convertase family, is an important drug target because of its crucial role in lipid metabolism. Emerging evidence suggests a direct role of localized PCSK9 in the pathogenesis of vascular diseases. With this in our consideration, we reviewed PCSK9 physiology with respect to recent development and major studies (clinical and experimental) on PCSK9 functionality in vascular disease. PCSK9 upregulates low-density lipoprotein (LDL)-cholesterol levels by binding to the LDL-receptor (LDLR) and facilitating its lysosomal degradation. PCSK9 gain-of-function mutations have been confirmed as a novel genetic mechanism for familial hypercholesterolemia. Elevated serum PCSK9 levels in patients with vascular diseases may contribute to coronary artery disease, atherosclerosis, cerebrovascular diseases, vasculitis, aortic diseases, and arterial aging pathogenesis. Experimental models of atherosclerosis, arterial aneurysm, and coronary or carotid artery ligation also support PCSK9 contribution to inflammatory response and disease progression, through LDLR-dependent or -independent mechanisms. More recently, several clinical trials have confirmed that anti-PCSK9 monoclonal antibodies can reduce systemic LDL levels, total nonfatal cardiovascular events, and all-cause mortality. Interaction of PCSK9 with other receptor proteins (LDLR-related proteins, cluster of differentiation family members, epithelial Na+ channels, and sortilin) may underlie its roles in vascular disease. Improved understanding of PCSK9 roles and molecular mechanisms in various vascular diseases will facilitate advances in lipid-lowering therapy and disease prevention.

Type 2 diabetes (T2DM) is a common comorbidity in patients with degenerative aortic stenosis (AS).As a key item of the American Society of Thoracic Surgeons (STS) score, it has a vital impact on the clinical prognosis of traditional thoracic surgery. T2DM has an adverse effect on the morbidity and mortality of cardiovascular diseases. At the same time, studies have shown that T2DM are associated with myocardial hypertrophy and remodeling, decreased left ventricular function, and worsening heart failure symptoms in the AS patients. Transcatheter aortic valve replacement (TAVR) as an interventional method to replace the aortic valve has better safety for middle and high risk patients in surgery, but the impact of T2DM on the clinical outcome of TAVR in AS patients is not clear.By analyzing the clinical and image characteristics of patients with AS and T2DM who received TAVR treatment, so as to explore the effect of T2DM on the perioperative complications and prognosis of TAVR.A total of 100 consecutive patients with severe AS, who underwent TAVR treatment and were followed up for more than 1 month, were selectedin the Second Xiangya Hospital of Central South University from January 2016 to December 2020.Among them, 5 patients who were treated with TAVR due to simple severe aortic regurgitation were not included, therefore a total of 95 patients with severe aortic stenosis were enrolled in this study.The age of the patients was (72.7±4.8) years old, and there were 58 males (61.1%), and the patients with moderate or above aortic regurgitation had 30 cases (31.6%). The patients were divided into a diabetic group and a non-diabetic group according to whether they were combined with T2DM.There was no statistical difference in age, gender, body mass index (BMI), STS score, and New York Heart Association (NYHA) cardiac function classification between the 2 groups (allCompared with the non-diabetic group, the diabetic group had high blood pressure and chronic renal insufficiency.There was no significant difference in preoperative ultrasound echocardiography between the 2 groups. Preoperative CT evaluation found that the anatomical structure of the aortic root in the diabetic group was smaller than that in the non-diabetic group, and there was no significant difference in the incidence of bicuspid aortic valve between the 2 groups (allT2DM is a risk factor for short-term poor prognosis in patients with symptomatic severe AS after TAVR treatment. T2DM should play an important role in the future construction of the TAVR surgical risk assessment system, but the conclusions still need to be further verified by long-term follow-up of large-scale clinical studies.

This study was conducted to investigate the effects of magnesium (Mg) supplementation on the growth performance, muscle fiber development and flesh quality of Megalobrama amblycephala fed a high-carbohydrate (CHO) diet. In vivo, six experimental diets, a control diet (30% CHO, C), and five Mg supplementation levels (0 (HC1), 200 (HC2), 400 (HC3), 800 (HC4) and 1200 (HC5) mg kg−1, respectively) of high-CHO diet (45% CHO), were formulated and then fed to M. amblycephala (initial weight 43.15 ± 0.43 g) for 13 weeks. Results showed that the HC1 diets remarkably decreased weight gain rate (WGR), specific growth rate (SGR), water holding capacity (WHC), pH 24 h postmortem, collagen content, textural properties (hardness, tenderness, chewiness and resilience), muscle fiber density, succinate dehydrogenase (SDH) and malate dehydrogenase (MDH) activities, as well as transcriptions of ampkα2, pgc-1α, mrf-4, myf-5 and myf-6 compared with the C group, but muscle AMP/ATP ratio, ATPase activities and mstna and mstnb transcription showed an opposite trend. The HC3 group of fish obtained relatively high values of WGR, SGR, muscle lipid and protein content, collagen content, textural properties (hardness, tenderness, chewiness and resilience), fiber density, SDH and MDH activities, AMP/ATP ratio as well as transcriptions of ampkα1, pgc-1α, myod, myog and myf-5 compared with other HC groups. In vitro, the isolated primary hepatocytes from M. amblycephala were assigned into four experimental groups: a control group (5.5 mM glucose, Control), a high glucose group (30 mM glucose, HG), an AICAR group (30 mM glucose + 250 μM AICAR, HGA) and an MgSO4 group (30 mM glucose + 2 mM MgSO4, HGM). Results showed that MgSO4 treatment remarkably increased p-Ampk/t-Ampk ratio, Pgc-1α protein content and transcriptions of ampkα1, ampkα2 and pgc-1α compared with the HG group. Overall, based on regression analysis for SGR, the optimal Mg level of M. amblycephala fed high-CHO diets was 366.67 mg kg-1, which was consistent with the above results that fish fed HC3 diets displayed higher the growth performance, muscle fiber density and flesh quality of M. amblycephala.

C54H58N6O16Pb2, triclinic, P 1 ‾ $P‾{1}$ (no. 2), a = 9.4690(6) Å, b = 12.9374(6) Å, c = 13.2303(7) Å, V = 1341.90(15) Å3, α = 63.395(5)°, β = 74.291(5)°, γ = 69.113(5)°, Z = 1, R gt (F) = 0.0284, wR ref(F 2) = 0.0484, T = 150 K.

C24H23N2NaO4, monoclinic, P21/c (no. 14), a = 7.5246(5) Å, b = 22.554(2) Å, c = 11.3358(9) Å, β = 91.881(7)°,V = 1922.8(3) Å3, Z = 4, Rgt(F) = 0.0496, wRref(F2) = 0.1184, T = 100K.