Hg4(Te2O5)(SO4): A Giant Birefringent Sulfate Crystal Triggered by a Highly Selective Cation.

Sulfate crystals are often criticized for their low birefringence. The small anisotropic SO4 group is becoming the biggest bottleneck hindering the application of sulfates in optical functional materials. In this study, we report a new method to significantly enhance the birefringence of sulfates. The title compound increases the birefringence recording of sulfates to 0.542@546 nm, which is significantly larger than that of the commercial birefringent crystal of TiO2 (0.306@546.1 nm). At the infrared wavelength, the birefringence of Hg4(Te2O5)(SO4) can be up to 0.400@1064 nm, which is also much larger than the infrared birefringent crystal of YVO4 (0.209@1064 nm). In addition, it also has a wide transparency range, high thermal stability, and excellent environmental stability, making it a potential birefringent material. Hg4(Te2O5)(SO4) features a novel two-dimensional layered structure composed of [Hg4(Te2O5)]2+ layers separated by isolated (SO4)2- tetrahedra. This compound was designed by introducing a highly selective cation in a tellurite sulfate system. The low valence low coordination cations connect with tellurite groups only, making the sulfate isolated in the structure. The steric repulsive action of the isolated SO4 tetrahedra may regulate the linear and lone pair groups arranged in a way that favors large birefringence. This method can be proven by theoretical calculations. PAWED studies showed that the large birefringence originated from the synergistic effect of (Hg2O2)2-, (Te2O5)2-, and (SO4)2- units, with a contribution ratio of 42.17, 37.92, and 19.88%, respectively. Our work breaks the limitation of low birefringence in sulfates and opens up new possibilities for their application as birefringent crystals.

UV-Transparent SHG Material Explored in an Alkali Metal Sulfate Selenite System.

The first examples of alkali metal selenite sulfates, namely, Na8(SeO3)(SO4)3 (1), Na2(H2SeO3)(SO4) (2), and K4(H2SeO3)(HSO4)2(SO4) (3), were successfully synthesized by hydrothermal reactions. Their structures display three different zero-dimensional configurations composed of isolated sulfate tetrahedra and selenite groups separated by alkali metals. Na8(SeO3)(SO4)3 (1) features a noncentrosymmetric structure, while Na2(H2SeO3)(SO4) (2) and K4(H2SeO3)(HSO4)2(SO4) (3) are centrosymmetric. Powder second-harmonic-generation measurements revealed that Na8(SeO3)(SO4)3 (1) shows a phase-matchable SHG intensity about 1.2 times that of KDP. UV-vis-NIR diffuse reflectance spectroscopic analysis indicated that Na8(SeO3)(SO4)3 (1) has a short UV cutoff edge and a large optical band gap, which makes it a possible UV nonlinear optical material. Theoretical calculations revealed that the birefringence of Na8(SeO3)(SO4)3 (1) is 0.041 at 532 nm, which is suitable for phase-matching condition. This work provides a good experimental foundation for the exploration of new UV nonlinear crystals in an alkali metal selenite sulfate system.

Nitrogen-doped titanium dioxide/schwertmannite nanocomposites as heterogeneous photo-Fenton catalysts with enhanced efficiency for the degradation of bisphenol A.

Potential health risks related to environmental endocrine disruptors (EEDs) have aroused research hotspots at the forefront of water treatment technologies. Herein, nitrogen-doped titanium dioxide/schwertmannite nanocomposites (N-TiO2/SCH) have been successfully developed as heterogeneous catalysts for the degradation of typical EEDs via photo-Fenton processes. Due to the sustainable Fe(III)/Fe(II) conversion induced by photoelectrons, as-prepared N-TiO2/SCH nanocomposites exhibit much enhanced efficiency for the degradation of bisphenol A (BPA; ca. 100% within 60 min under visible irradiation) in a wide pH range of 3.0-7.8, which is significantly higher than that of the pristine schwertmannite (ca. 74.5%) or N-TiO2 (ca. 10.8%). In this photo-Fenton system, the efficient degradation of BPA is mainly attributed to the oxidation by hydroxyl radical (•OH) and singlet oxygen (1O2). Moreover, the possible catalytic mechanisms and reaction pathway of BPA degradation are systematically investigated based on analytical and photoelectrochemical analyses. This work not only provides a feasible means for the development of novel heterogeneous photo-Fenton catalysts, but also lays a theoretical foundation for the potential application of mineral-based materials in wastewater treatment.

K3ZrF4(SbF4)(SbF5) and K8(ZrF6)(Sb2Zr2F20): Two Zirconium Fluoroantimonites with Low Dimensional Structures and Wide Transparency Range.

The first examples of zirconium fluoroantimonites, namely, K3ZrF4(SbF4)(SbF5) and K8(ZrF6)(Sb2Zr2F20), have been successfully synthesized by facial hydrothermal reactions. K3ZrF4(SbF4)(SbF5) features a unique 1D (ZrSb2F13)3- double-chain structure, while K8(ZrF6)(Sb2Zr2F20) displays a special 0D construction composed of Zr2Sb2F20 tetranuclear clusters and isolated ZrF6 octahedra. The two fluorides can exhibit a broad transparency range with almost no absorption peaks from ultraviolet to near-IR. For K8(ZrF6)(Sb2Zr2F20), a phase transformation was found before decomposition. The band structures, density of states, and linear-optical properties for the title compounds were also obtained.

Predicting the effect of sirolimus on disease activity in patients with systemic lupus erythematosus using machine learning.

WHAT IS KNOWN AND OBJECTIVES: The present study aimed to predict the effect of sirolimus on disease activity in patients with systemic lupus erythematosus (SLE) using machine learning and to recommend appropriate sirolimus dosage regimen for patients with SLE. METHODS: The Emax model was selected for machine learning, where the evaluation indicator was the change rate of systemic lupus erythematosus disease activity index from baseline value. RESULTS: A total 103 patients with SLE were included for modelling, where the Emax , ET50 were -53.9%, 1.53 months in the final model respectively, and the evaluation of the final model was good. Further simulation found that the follow-up time to achieve 25%, 50%, 75% and 80% (plateau) Emax of sirolimus effecting on disease activity in patients with SLE were 0.51, 1.53, 4.59 and 6.12 months, respectively. In addition, the sirolimus dosage was flexible and adjusted according to drug concentration, where the intersection of sirolimus concentration range included in this study was about 8-10 ng/ml. WHAT IS NEW AND CONCLUSIONS: This study was the first time to predict the effect of sirolimus on disease activity in patients with SLE and in order to achieve better therapeutic effect maintaining a concentration of 8-10 ng/ml sirolimus for at least 6.12 months was necessary.

Urotensin II and urantide exert opposite effects on the cellular components of atherosclerotic plaque in hypercholesterolemic rabbits.

Increasing levels of plasma urotensin II (UII) are positively associated with atherosclerosis. In this study we investigated the role of macrophage-secreted UII in atherosclerosis progression, and evaluated the therapeutic value of urantide, a potent competitive UII receptor antagonist, in atherosclerosis treatment. Macrophage-specific human UII-transgenic rabbits and their nontransgenic littermates were fed a high cholesterol diet for 16 weeks to induce atherosclerosis. Immunohistochemical staining of the cellular components (macrophages and smooth muscle cells) of aortic atherosclerotic lesions revealed a significant increase (52%) in the macrophage-positive area in only male transgenic rabbits compared with that in the nontransgenic littermates. However, both male and female transgenic rabbits showed a significant decrease (45% in males and 31% in females) in the smooth muscle cell-positive area compared with that of their control littermates. The effects of macrophage-secreted UII on the plaque cellular components were independent of plasma lipid level. Meanwhile the wild-type rabbits were continuously subcutaneously infused with urantide (5.4 µg· kg-1· h-1) using osmotic mini-pumps. Infusion of urantide exerted effects opposite to those caused by UII, as it significantly decreased the macrophage-positive area in male wild-type rabbits compared with that of control rabbits. In cultured human umbilical vein endothelial cells, treatment with UII dose-dependently increased the expression of the adhesion molecules VCAM-1 and ICAM-1, and this effect was partially reversed by urantide. The current study provides direct evidence that macrophage-secreted UII plays a key role in atherogenesis. Targeting UII with urantide may promote plaque stability by decreasing macrophage-derived foam cell formation, which is an indicator of unstable plaque.

MicroRNA-155 Deficiency Leads to Decreased Atherosclerosis, Increased White Adipose Tissue Obesity, and Non-alcoholic Fatty Liver Disease: A NOVEL MOUSE MODEL OF OBESITY PARADOX.

Obesity paradox (OP) describes a widely observed clinical finding of improved cardiovascular fitness and survival in some overweight or obese patients. The molecular mechanisms underlying OP remain enigmatic partly due to a lack of animal models mirroring OP in patients. Using apolipoprotein E knock-out (apoE-/-) mice on a high fat (HF) diet as an atherosclerotic obesity model, we demonstrated 1) microRNA-155 (miRNA-155, miR-155) is significantly up-regulated in the aortas of apoE-/- mice, and miR-155 deficiency in apoE-/- mice inhibits atherosclerosis; 2) apoE-/-/miR-155-/- (double knock-out (DKO)) mice show HF diet-induced obesity, adipocyte hypertrophy, and present with non-alcoholic fatty liver disease; 3) DKO mice demonstrate HF diet-induced elevations of plasma leptin, resistin, fed-state and fasting insulin and increased expression of adipogenic transcription factors but lack glucose intolerance and insulin resistance. Our results are the first to present an OP model using DKO mice with features of decreased atherosclerosis, increased obesity, and non-alcoholic fatty liver disease. Our findings suggest the mechanistic role of reduced miR-155 expression in OP and present a new OP working model based on a single miRNA deficiency in diet-induced obese atherogenic mice. Furthermore, our results serve as a breakthrough in understanding the potential mechanism underlying OP and provide a new biomarker and novel therapeutic target for OP-related metabolic diseases.

Interleukin-17A Promotes Aortic Endothelial Cell Activation via Transcriptionally and Post-translationally Activating p38 Mitogen-activated Protein Kinase (MAPK) Pathway.

Interleukin-17 (IL-17)-secreting T helper 17 cells were recently identified as a CD4(+) T helper subset and implicated in various inflammatory and autoimmune diseases. The issues of whether and by what mechanism hyperlipidemic stress induces IL-17A to activate aortic endothelial cells (ECs) and enhance monocyte adhesion remained largely unknown. Using biochemical, immunological, microarray, experimental data mining analysis, and pathological approaches focused on primary human and mouse aortic ECs (HAECs and MAECs) and our newly generated apolipoprotein E (ApoE)(-/-)/IL-17A(-/-) mice, we report the following new findings. 1) The hyperlipidemia stimulus oxidized low density lipoprotein up-regulated IL-17 receptor(s) in HAECs and MAECs. 2) IL-17A activated HAECs and increased human monocyte adhesion in vitro. 3) A deficiency of IL-17A reduced leukocyte adhesion to endothelium in vivo. 3) IL-17A activated HAECs and MAECs via up-regulation of proinflammatory cytokines IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), chemokine CXC motif ligand 1 (CXCL1), and CXCL2. 4) IL-17A activated ECs specifically via the p38 mitogen-activated protein kinases (MAPK) pathway; the inhibition of p38 MAPK in ECs attenuated IL-17A-mediated activation by ameliorating the expression of the aforementioned proinflammatory cytokines, chemokines, and EC adhesion molecules including intercellular adhesion molecule 1. Taken together, our results demonstrate for the first time that IL-17A activates aortic ECs specifically via p38 MAPK pathway.

Inhibition of Caspase-1 Activation in Endothelial Cells Improves Angiogenesis: A NOVEL THERAPEUTIC POTENTIAL FOR ISCHEMIA.

Deficient angiogenesis may contribute to worsen the prognosis of myocardial ischemia, peripheral arterial disease, ischemic stroke, etc. Dyslipidemic and inflammatory environments attenuate endothelial cell (EC) proliferation and angiogenesis, worsening the prognosis of ischemia. Under these dyslipidemic and inflammatory environments, EC-caspase-1 becomes activated and induces inflammatory cell death that is defined as pyroptosis. However, the underlying mechanism that correlates caspase-1 activation with angiogenic impairment and the prognosis of ischemia remains poorly defined. By using flow cytometric analysis, enzyme and receptor inhibitors, and hind limb ischemia model in caspase-1 knock-out (KO) mice, we examined our novel hypothesis, i.e. inhibition of caspase-1 in ECs under dyslipidemic and inflammatory environments attenuates EC pyroptosis, improves EC survival mediated by vascular endothelial growth factor receptor 2 (VEGFR-2), angiogenesis, and the prognosis of ischemia. We have made the following findings. Proatherogenic lipids induce higher caspase-1 activation in larger sizes of human aortic endothelial cells (HAECs) than in smaller sizes of HAECs. Proatherogenic lipids increase pyroptosis significantly more in smaller sizes of HAECs than in larger sizes of the cells. VEGFR-2 inhibition increases caspase-1 activation in HAECs induced by lysophosphatidylcholine treatment. Caspase-1 activation inhibits VEGFR-2 expression. Caspase-1 inhibition improves the tube formation of lysophosphatidylcholine-treated HAECs. Finally, caspase-1 depletion improves angiogenesis and blood flow in mouse hind limb ischemic tissues. Our results have demonstrated for the first time that inhibition of proatherogenic caspase-1 activation in ECs improves angiogenesis and the prognosis of ischemia.

A simple and biosafe method for isolation of human umbilical vein endothelial cells.

Human umbilical vein endothelial cells (HUVECS) are used as an irreplaceable tool for the study of vascular diseases. However, the technicians who isolate HUVECs are largely exposed to potential infectious threats. Here we report the development of a specialized instrument to protect researchers from known or unknown infectious agents when they operate on human umbilical cords. This instrument can be assembled by common laboratory supplies and adapted to accommodate umbilical cords of different lengths. When the cord is enclosed within the instrument, the risk of sample contamination and operator infection is greatly reduced. Using our instrument, endothelial cells were successfully isolated from human umbilical veins without contamination. The cells were verified by their cobblestone-like morphology and by immunofluorescence staining (Factor VIII and CD31 positivity and α-SMA negativity). Our instrument simplifies and optimizes the cell extraction process, and most importantly elevates the biosafety to a higher level during the isolation of human umbilical vein endothelial cells.

Early hyperlipidemia promotes endothelial activation via a caspase-1-sirtuin 1 pathway.

OBJECTIVE: The role of receptors for endogenous metabolic danger signals-associated molecular patterns has been characterized recently as bridging innate immune sensory systems for danger signals-associated molecular patterns to initiation of inflammation in bone marrow-derived cells, such as macrophages. However, it remains unknown whether endothelial cells (ECs), the cell type with the largest numbers and the first vessel cell type exposed to circulating danger signals-associated molecular patterns in the blood, can sense hyperlipidemia. This report determined whether caspase-1 plays a role in ECs in sensing hyperlipidemia and promoting EC activation. APPROACH AND RESULTS: Using biochemical, immunologic, pathological, and bone marrow transplantation methods together with the generation of new apoplipoprotein E (ApoE)(-/-)/caspase-1(-/-) double knockout mice, we made the following observations: (1) early hyperlipidemia induced caspase-1 activation in ApoE(-/-) mouse aorta; (2) caspase-1(-/-)/ApoE(-/-) mice attenuated early atherosclerosis; (3) caspase-1(-/-)/ApoE(-/-) mice had decreased aortic expression of proinflammatory cytokines and attenuated aortic monocyte recruitment; and (4) caspase-1(-/-)/ApoE(-/-) mice had decreased EC activation, including reduced adhesion molecule expression and cytokine secretion. Mechanistically, oxidized lipids activated caspase-1 and promoted pyroptosis in ECs by a reactive oxygen species mechanism. Caspase-1 inhibition resulted in accumulation of sirtuin 1 in the ApoE(-/-) aorta, and sirtuin 1 inhibited caspase-1 upregulated genes via activator protein-1 pathway. CONCLUSIONS: Our results demonstrate for the first time that early hyperlipidemia promotes EC activation before monocyte recruitment via a caspase-1-sirtuin 1-activator protein-1 pathway, which provides an important insight into the development of novel therapeutics for blocking caspase-1 activation as early intervention of metabolic cardiovascular diseases and inflammations.

Low serum ficolin-3 levels are associated with severity and poor outcome in traumatic brain injury.

BACKGROUND: Ficolin-mediated activation of the lectin pathway of complement contributes to the complement-independent inflammatory processes of traumatic brain injury. Lower serum ficolin-3 levels have been demonstrated to be highly associated with unfavorable outcome after ischemic stroke. This prospective observatory study was designed to investigate the relationships between serum ficolin-3 levels and injury severity and clinical outcomes after severe traumatic brain injury. METHODS: Serum ficolin-3 levels of 128 patients and 128 healthy controls were measured by sandwich immunoassays. An unfavorable outcome was defined as Glasgow Outcome Scale score of 1-3. Study endpoints included mortality at 1 week and 6 months and unfavorable outcome at 6 months after head trauma. Injury severity was assessed by Glasgow Coma Scale score. Multivariate logistic models were structured to evaluate the relationships between serum ficolin-3 levels and study endpoints and injury severity. RESULTS: Compared with the healthy controls, serum ficolin-3 levels on admission were statistically decreased in patients with severe traumatic brain injury. Serum ficolin-3 levels were independently correlated with Glasgow Coma Scale scores. Ficolin-3 was also identified as an independent prognostic predictor for 1-week mortality, 6-month mortality, and 6-month unfavorable outcome. Under receiver operating characteristics curves, ficolin-3 has similar prognostic predictive values for all study endpoints compared with Glasgow Coma Scale scores. CONCLUSIONS: It was proposed that lower serum ficolin-3 levels, correlated with injury severity, had the potential to be the useful, complementary tool to predict short- or long-term clinical outcomes after severe traumatic brain injury.

[(C5H6N2)2H](Sb4F13): a polyfluoroantimonite with a strong second harmonic generation effect.

It is of great difficulty to create a new antimonite with second-harmonic-generation (SHG) intensity larger than 6 times that of KDP. In this study, a polyfluoroantimonite strategy has been proposed to explore fluoroantimonites with large nonlinear optical (NLO) coefficients. Under the cooperation of chemical (highly asymmetric π-conjugated organic amine) and physical (viscous reaction medium ethylene glycol) methods, two novel polyfluoroantimonites, namely, (3PC)2(Sb4F14) and (3AP)2(Sb4F13), have been achieved. Interestingly, these two structures contain two new polyfluoroantimonite groups respectively, an isolated (Sb4F14)2- four-member polyhedral ring and an infinite [Sb4F13]∞- helical chain. More importantly, the polar (3AP)2(Sb4F13) displays a strong SHG intensity of 8.1 × KDP, a large birefringence of 0.258@546 nm and a high laser-induced damage threshold (LIDT) value of 149.7 MW cm-2. Theoretical calculations indicated that its strong SHG effect stems from the synergistic effect of the helical [Sb4F13]∞- polyfluoroantimonite chain and π-conjugated 3AP+ cation, with a contribution ratio of 48.93% and 50.77% respectively. This work provides a new approach for the design and synthesis of high-performance fluoroantimonites.

Effects of dapagliflozin on body weight in patients with type 2 diabetes mellitus: Evidence­based practice.

The dose-dependent pharmacological response to dapagliflozin in patients with type 2 diabetes mellitus (T2DM) with regard to weight loss remain unknown. The aim of the present study was to investigate the effects of dapagliflozin on weight loss in patients with T2DM. A total of 8,545 patients with T2DM from 24 randomized controlled trials reported in the literature were selected for inclusion in the study. Data from these trials were analyzed using maximal effect (Emax) models with nonlinear mixed effects modeling; the evaluation index was the body weight change rate from baseline values. Patients treated with 2.5 mg/day dapagliflozin exhibited an Emax of -3.04%, and the time taken for therapy to reach half of the Emax (ET50) was estimated to be 30.8 weeks for patients treated with this dose. Patients treated with 5, 10 and 20 mg/day dapagliflozin exhibited Emax values of -6.57, -4.12 and -3.23%, respectively, and their ET50 values were estimated to be 27.3, 20.4 and 4.23 weeks, respectively. The data indicated ideal linear relationships between individual predictions and observations, suggesting the optimal fitting of the final models. The present study is the first systematic analysis of the effect of dapagliflozin on weight loss in patients with T2DM. The application of dapagliflozin at 5 mg/day exhibited a greater weight loss effect compared with the other doses used, and the weight loss onset time shortened as the dose of dapagliflozin increased.

The Dosage Recommendation of Cyclosporin in Children with Hemophagocytic Lymphohistiocytosis based on Population Pharmacokinetic Model.

OBJECTIVES: Cyclosporin is one of the therapeutic regimens for hemophagocytic lymphohistiocytosis (HLH); however, the optimal dosage of cyclosporine in children with HLH is unknown. It has been found that piperacillin-tazobactam affects the cyclosporine pharmacokinetic process in pediatric HLH patients. Thus, the purpose of the present study was to recommend cyclosporin dosage for pediatric HLH with and without piperacillin- tazobactam. METHODS: A previously established cyclosporine population pharmacokinetic model for pediatric HLH patients has been used in this study to recommend optimal dosage based on Monte Carlo simulation. The pediatric HLH patients have been included in eight weight groups (5, 10, 20, 30, 40, 50, 60, 70 kg) for sixteen dosages (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16 mg/kg), split into one dose or two doses. RESULTS: The optimal cyclosporin dosages for children having HLH without piperacillin-tazobactam have been found to be 15, 13, 12, 11, 10, and 9 mg/kg, split into two doses for weights of 5-7, 7-10, 10-20, 20-28, 28-45, and 45-70 kg, respectively. For children with HLH, optimal cyclosporin dosages with piperacillin-tazobactam have been found to be 8 and 7 mg/kg, split into two doses for weights of 5-20 and 20-70 kg, respectively. CONCLUSION: It is the first time that the cyclosporin dosage regimens for HLH in children have been developed based on Monte Carlo simulation, and the initial dosage optimizations of cyclosporine in pediatric HLH patients have been recommended.

Maternal vitamin B1 is a determinant for the fate of primordial follicle formation in offspring.

The mediation of maternal-embryonic cross-talk via nutrition and metabolism impacts greatly on offspring health. However, the underlying key interfaces remain elusive. Here, we determined that maternal high-fat diet during pregnancy in mice impaired preservation of the ovarian primordial follicle pool in female offspring, which was concomitant with mitochondrial dysfunction of germ cells. Furthermore, this occurred through a reduction in maternal gut microbiota-related vitamin B1 while the defects were restored via vitamin B1 supplementation. Intriguingly, vitamin B1 promoted acetyl-CoA metabolism in offspring ovaries, contributing to histone acetylation and chromatin accessibility at the promoters of cell cycle-related genes, enhancement of mitochondrial function, and improvement of granulosa cell proliferation. In humans, vitamin B1 is downregulated in the serum of women with gestational diabetes mellitus. In this work, these findings uncover the role of the non-gamete transmission of maternal high-fat diet in influencing offspring oogenic fate. Vitamin B1 could be a promising therapeutic approach for protecting offspring health.

catena-Poly[[[aqua-(2,2'-bipyridine-κ(2) N,N')zinc]-µ-furan-2,5-dicarboxyl-ato-κ(2) O (2):O (5)] dihydrate].

In the title hydrated coordination polymer, {[Zn(C6H2O5)(C10H8N2)(H2O)]·2H2O} n , an infinite [1-10] chain is formed by the linking of [Zn(C10H8N2)(H2O)](2+) entities by bridging, monodentate furan-2,5-dicarboxyl-ate dianionic linkers. The Zn(2+) coordination geometry is a trigonal bipyramid, with one N atom (from 2,2'-bipyridine) and one O atom (from the bridging dianion) in the axial positions. For each Zn(II) atom, the dihedral angle between the furan ring of its coordinated bridging ligand and its coordinated bipyridine ring system is 87.19 (8)°. O-H⋯O hydrogen bonds involving both the coordinated and uncoordinated water mol-ecules generate a layer motif parallel to (001).

Poly[[µ-aqua-diaqua-bis-(µ-furan-2,5-dicarboxyl-ato-κ(2) O (2):O (5))bis-(1,10-phenanthroline-κ(2) N,N')dicopper(II)] N,N-dimethyl-formamide monosolvate].

The asymmetric unit of the title compound, {[Cu2(C6H2O5)2(C12H8N2)2(H2O)3]·C3H7NO} n , contains two Cu(II) atoms, two furan-2,5-dicarboxyl-ate (L) ligands, two 1,10-phenanthroline (phen) ligands, three coordinating water mol-ecules and one N,N-dimethyl-formamide solvent mol-ecule. Each Cu(II) atom is coordinated by two N atoms from one phen ligand, two O atoms from two L ligands and two water mol-ecules in a distorted octa-hedral geometry. The main difference between the environments of the two independent Cu atoms is in the Cu-Owater distances, which are 2.415 (2) and 2.639 (2) Šfor one Cu(II) atom and 2.3560 (19) and 2.911 (4) Šfor the other. Ligands L and one independent water mol-ecule bridge the Cu(II) atoms, forming corrugated polymeric layers parallel to the ab plane. Inter-molecular O-H⋯O and C-H⋯O hydrogen bonds consolidate the crystal packing.

catena-Poly[[[aqua-(2,2'-bipyridine-κ(2)N,N')copper(II)]-µ-furan-2,5-di-carboxyl-ato-κ(2)O(2):O(5)] dihydrate].

In the crystal structure of the title compound, {[Cu(C(6)H(2)O(5))(C(10)H(8)N(2))(H(2)O)]·2H(2)O}(n), an infinite chain parallel to [110] is formed by the linking of Cu(H(2)O)(2,2'-bipyridine) units through a furan-2,5-dicarboxyl-ate bridge. The Cu(II) atom shows a square-pyramidal geometry, with one furan-2,5-dicarboxyl-ate O atom in the apical position. The dihedral angle between the planes of the furan ring and the bipyridine mol-ecule is 83.88 (7)°. O(water)-H⋯O hydrogen bonds connect adjacent chains, generating a layer motif parallel to (001).