A series of pure-blue-light emitting Cu(i) complexes with thermally activated delayed fluorescence: structural, photophysical, and computational studies.

Four mononuclear Cu(i)-halide complexes containing phosphines and pyridine ligands with strong electron donor substituents, [CuCl(PPh3)2(4-NMe2py)] (1), [CuI(PPh3)2(4-NH2py)] (2), [CuI(POP)(4-NH2py)] (3), and [CuI(POP)(4-NMe2py)]·0.5(Et2O) (4), (PPh3 = triphenylphosphine, 4-NMe2py = 4-(dimethylamino)pyridine, POP = bis[(2-diphenyl-phosphino)phenyl]ether, 4-NH2py = 4-aminopyridine, Et2O = diethyl ether) were synthesized and studied with regard to their structural, photophysical properties and theoretical calculations. The complexes exhibit pure blue thermally activated delayed fluorescence (λmax = 442 (1), 436 (2), 464 (3), and 448 nm (4)) in crystalline at room temperature. Emission lifetime analyses and density functional theory (DFT) calculations show that the blue-light emission at room temperature is the singlet (metal + halide)-to-ligand charge transfer state, (1(M + X)LCT), while that at 77 K is the state of 3(M + X)LCT transition character, owing to the small singlet-triplet energy gaps (ΔE = 660-1680 cm-1). X-ray diffraction structure analysis, photophysical studies and theoretical calculations suggest that the much larger torsion angle between the N-heterocyclic rings and N-Cu-X planes of complex 3 than that of 1, 2 and 4 might causes the bathochromic shift of luminescence, although these complexes containing similar heterocycle ligands.

A two-dimensional silver(I) coordination polymer constructed from 4-aminophenylarsonate and triphenylphosphane: poly[[(µ3-4-aminophenylarsonato-κ³N:O:O)(triphenylphosphane-κP)silver(I)] monohydrate].

The title compound, {[Ag(C6H7AsNO3)(C18H15P)]·H2O}n, has been synthesized from the reaction of 4-aminophenylarsonic acid with silver nitrate, in aqueous ammonia, with the addition of triphenylphosphane (PPh3). The Ag(I) centre is four-coordinated by one amino N atom, one PPh3 P atom and two arsonate O atoms, forming a severely distorted [AgNPO2] tetrahedron. Two Ag(I)-centred tetrahedra are held together to produce a dinuclear [Ag2O2N2P2] unit by sharing an O-O edge. 4-Aminophenylarsonate (Hapa(-)) adopts a µ3-κ(3)N:O:O-tridentate coordination mode connecting two dinuclear units, resulting in a neutral [Ag(Hapa)(PPh3)]n layer lying parallel to the (101̄) plane. The PPh3 ligands are suspended on both sides of the [Ag(Hapa)(PPh3)]n layer, displaying up and down orientations. There is an R2(2)(8) hydrogen-bonded dimer involving two arsonate groups from two Hapa(-) ligands related by a centre of inversion. Additionally, there are hydrogen-bonding interactions involving the solvent water molecules and the arsonate and amine groups of the Hapa(-) ligands, and weak π-π stacking interactions within the [Ag(Hapa)(PPh3)]n layer. These two-dimensional layers are further assembled by weak van der Waals interactions to form the final architecture.

A three-dimensional coordination polymer based on the Zn4(µ3-OH)2 unit: poly[[(µ4-benzene-1,4-dicarboxylato)bis(µ3-benzene-1,4-dicarboxylato)bis(µ3-hydroxido)bis(1,10-phenanthroline-5,6-dione)tetrazinc] dihydrate].

The title compound, {[Zn4(C8H4O4)3(OH)2(C12H6N2O2)2]·2H2O}n, has been prepared hydrothermally by the reaction of Zn(NO3)2·6H2O with benzene-1,4-dicarboxylic acid (H2bdc) and 1,10-phenanthroline-5,6-dione (pdon) in H2O. In the crystal structure, a tetranuclear Zn4(OH)2 fragment is located on a crystallographic inversion centre which relates two subunits, each containing a [ZnN2O4] octahedron and a [ZnO4] tetrahedron bridged by a µ3-OH group. The pdon ligand chelates to zinc through its two N atoms to form part of the [ZnN2O4] octahedron. The two crystallographically independent bdc(2-) ligands are fully deprotonated and adopt µ3-κO:κO':κO'' and µ4-κO:κO':κO'':κO''' coordination modes, bridging three or four Zn(II) cations, respectively, from two Zn4(OH)2 units. The Zn4(OH)2 fragment connects six neighbouring tetranuclear units through four µ3-bdc(2-) and two µ4-bdc(2-) ligands, forming a three-dimensional framework with uninodal 6-connected α-Po topology, in which the tetranuclear Zn4(OH)2 units are considered as 6-connected nodes and the bdc(2-) ligands act as linkers. The uncoordinated water molecules are located on opposite sides of the Zn4(OH)2 unit and are connected to it through hydrogen-bonding interactions involving hydroxide and carboxylate groups. The structure is further stabilized by extensive π-π interactions between the pdon and µ4-bdc(2-) ligands.

Predictors of liver failure in primary biliary cirrhosis.

BACKGROUND: The disease progression of patients with primary biliary cirrhosis (PBC) varies significantly, and the prognostic markers that identify those patients who will develop liver failure have been scarcely studied from a Chinese cohort. Aims. We aimed to determine the predictive factors of liver failure in patients with PBC. METHODS: Patients who were first diagnosed as PBC with hepatic compensation between January 2007 and December 2009 were enrolled in this cohort study. RESULTS: Altogether 398 patients were finally included. Of these patients, 80% were women, 98% had positive antimitochondrial antibodies, and 45% had positive antinuclear antibodies (ANA). To December 2012, a total of 38 patients developed liver failure. According to the outcome, patients who developed liver failure had had higher serum concentration of baseline total bilirubin (TBil) (p = 0.013) and total bile acid (TBA) (p < 0.001), and lower concentrations of baseline total cholesterol (Tch) (p = 0.008), than patients who did not develop liver failure. Additionally, the proportion of ANA positivity was statistically different between the two groups (p = 0.009). In the established model for predicting liver failure in PBC, three variables were finally selected out, including Tch (odds ratio (OR) 0.552, 95% confidence interval (CI) 0.394-0.774, p < 0.001), TBA (OR 1.006, 95% CI 1.002-1.010, p = 0.002), and ANA (+ versus -, OR 5.518, 95% CI 1.155-26.376, p = 0.032). CONCLUSIONS: ANA, Tch, and TBA are predictors of liver failure in PBC.

Acute liver failure caused by severe acute hepatitis B: a case series from a multi-center investigation.

BACKGROUND: Few data can be available regarding acute liver failure (ALF) caused by severe acute hepatitis B up to now. This study aims to report such cases from China. FINDINGS: We conducted a multi-center investigation on ALF from 7 tertiary hospitals in different areas of China. A total of 11 patients with ALF caused by severe acute hepatitis B were finally identified. In these patients, there were 10 male and 1 female patients. As a serious complication, apparent hemorrhage occurred in 9 patients. Eventually, in these 11 patients, 4 survived and 7 died. 4 died of heavy bleeding, 2 died of systemic inflammatory response syndrome and 1 died of irreversible coma. No patients received liver transplantation. CONCLUSIONS: ALF caused by severe acute hepatitis B is worthy of formal studies based on its rarity and severity.

Acute liver failure in Chinese children: a multicenter investigation.

BACKGROUND: Currently, no documentation is available regarding Chinese children with acute liver failure (ALF). This study was undertaken to investigate etiologies and outcomes of Chinese children with ALF. METHODS: We retrospectively enrolled 32 pediatric patients with ALF admitted in five hospitals in different areas of China from January 2007 to December 2012. The coagulation indices, serum creatinine, serum lactate dehydrogenase, blood ammonia and prothrombin activity were analyzed; the relationship between these indices and mortality was evaluated by multivariate analysis. RESULTS: The most common causes of Chinese children with ALF were indeterminate etiology (15/32), drug toxicity (8/32), and acute cytomegalovirus hepatitis (6/32). Only 1 patient (3.13%) received liver transplantation and the spontaneous mortality of Chinese children with ALF was 58.06% (18/31). Patients who eventually died had higher baseline levels of international normalized ratio (P=0.01), serum creatinine (P=0.04), serum lactate dehydrogenase (P=0.01), blood ammonia (P<0.01) and lower prothrombin activity (P=0.01) than those who survived. Multivariate analysis showed that the entry blood ammonia was the only independent factor significantly associated with mortality (odds ratio=1.069, 95% confidence interval 1.023-1.117, P<0.01) and it had a sensitivity of 94.74%, a specificity of 84.62% and an accuracy of 90.63% for predicting the death. Based on the established model, with an increase of blood ammonia level, the risk of mortality would increase by 6.9%. CONCLUSIONS: The indeterminate causes predominated in the etiologies of ALF in Chinese children. The spontaneous mortality of pediatric patients with ALF was high, whereas the proportion of patients undergoing liver transplantation was significantly low. Entry blood ammonia was a reliable predictor for the death of pediatric patients with ALF.

Omeprazole affects clopidogrel efficacy but not ischemic events in patients with acute coronary syndrome undergoing elective percutaneous coronary intervention.

BACKGROUND: Omeprazole, usually used in the antiplatelet therapy during percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS), has been reported to increase ischemic events in retrospective studies. However, other clinical trials gave paradoxical results. The aim of this study was to assess the effects of omeprazole on clopidogrel efficacy and clinical events. METHODS: All patients (n = 172) received aspirin (loading dose 300 mg and maintenance dose 100 mg/d) and clopidogrel (loading dose 600 mg and maintenance dose 75 mg/d) during the therapy. They were randomized to receive omeprazole (20 mg/d) or placebo for 30 days. Residual platelet activities in the adenosine 5'-diphosphate (ADP) pathway were detected on the fifth day after PCI with thrombelastography (TEG)-mapping. The clinical events were recorded after one month. RESULTS: According to the five levels of platelet activities, the frequency distributions of the inhibition rates were significantly different (P = 0.0062). However, no significant change was seen in the distribution among the highest or the lowest inhibiting levels (> 95% and < 30% inhibition rate). And there were no significant differences (P > 0.05) in events incidence, while gastro-intestinal bleeding decreased in co-administration of omeprazole. CONCLUSIONS: Omeprazole significantly blunts clopidogrel efficacy while not exacerbates ischemic events in ACS undergoing PCI. Omeprazole even can decrease gastro-intestinal bleeding in those patients.