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AIM: To evaluate the protective mechanisms of piperine in the retina of mice with streptozotocin-induced diabetes. METHODS: In experiments in vitro, stimulation by chemical hypoxia was established in ARPE-19 cells. Then, the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor A (VEGFA), and pigment epithelium-derived factor (PEDF) was assessed at the mRNA and protein levels. In experiments in vivo, diabetes mellitus was established by intraperitoneally injecting 150 mg/kg streptozotocin once. After 3wk of the onset of diabetes, 15 mg/kg piperine was intraperitoneally injected once daily for 1 or 3wk. Then, the retinal morphology and mRNA and protein expression were assessed. RESULTS: In hypoxia, 1-100 μmol/L piperine significantly decreased the expression of VEGFA mRNA and increased the expression of PEDF mRNA without affecting HIF-1α mRNA. Meanwhile, 100 μmol/L piperine substantially decreased the protein level of VEGFA and increased the protein level of PEDF. The HIF-1α protein level was also hampered by piperine. In the diabetic retina of mice, the morphological damage was alleviated by piperine. Likewise, the retinal vascular leakage was substantially decreased by piperine. Further, the protein levels of HIF-1α and VEGFA were significantly reduced by piperine. Moreover, the level of the antiangiogenic factor of PEDF dramatically increased by piperine. CONCLUSION: Piperine may exert protective effects on the retina of mice with diabetes via regulating the pro-antiangiogenic homeostasis composed of HIF-1/VEGFA and PEDF.

Objective: Obesity is associated with an increased risk of developing insulin resistance and type 2 diabetes, since insulin can induce adipogenic differentiation of human adipose-derived stem cells (ADSCs). MiR-26a was reported to be highly expressed in ADSCs under induction and Forkhead box C2 (FOXC2), as a key substrate of cyclin-dependent kinase 5 (CDK5) could inhibit white adipocyte differentiation, which was mediated by miR-26a. However, the relationship between miR-26a and CDK5/FOXC2 during ADSCs differentiation remains unknown. We want to verify the regulated mechanism of miR-26a/CDK5/FOXC2 axis participating in the adipogenic differentiation of ADSCS. Methods: ADSCs were isolated and verified by flow cytometry. Oil Red O staining was performed to assess the capacity for adipogenic differentiation of ADSCs. The proliferation ability of ADSCs was verified by MTT assay. The expression of miR-26a, peroxisome proliferator-activated receptors γ (PPARγ), CDK5, and FOXC2 were tested by qRT-PCR and Western blot, and the relationship between miR-26a and CDK5 was verified by dual-luciferase reporter gene assay. Results: MiR-26a and PPARγ were upregulated and CDK5 and FOXC2 were downregulated during adipogenic differentiation of ADSCs. Knockdown of miR-26a or overexpression of CDK5 could inhibit adipogenic differentiation of ADSCs induced by insulin. MiR-26a could directly target CDK5 and the effect of miR-26a inhibitor on adipogenic differentiation of ADSCs could be blocked by si-CDK5. Conclusion: We demonstrated that miR-26a regulated insulin-induced adipogenic differentiation of ADSCs by regulating CDK5/FOXC2 pathway, which could provide the key to a comprehensive mechanistic understanding of obesity and type 2 diabetes.

Objective 1) To investigate the effect of FOXC2 on the differentiation of adipose-derived mesenchymal stem cells. 2) To analyze the mechanism between FOXC2 expression regulation in adipose differentiation and insulin resistance (IR). Methods We first amplified the FOXC2 promoter region-512 and cloned it into the luciferase expression vector. The reporter gene system was transfected into the adipose tissue-derived mesenchymal stem cell to study insulin-mediated FOXC2 expression. We also manipulated FOXC2 protein expression by either siRNA or overexpression and studied the differentiation capability of adipose tissue-derived mesenchymal stem cell into adipocytes, as well as the influence on several IR-related genes: GLUT4, PPARγ, UCP1 and PAI-1. Results 1) Insulin effectively induced the expression of FOXC2 protein in adipose tissue-derived mesenchymal stem cells under differentiation (P

PurposeAvailable data on the effects of anti-diabetic drugs on fracture risk are contradictory. Therefore, our study aimed to analyze all available data on the effects of anti-diabetic drugs on fracture risk in type 2 diabetes mellitus (T2DM) patients.MethodsEmbase, Medline, ClinicalTrials.gov, and Cochrane CENTRAL were searched for relevant trials. All data analyses were performed with STATA (12.0) and R language (3.6.0). Risk ratio (RR) with its 95% confidence interval (CI) was calculated by combining data for the fracture effects of anti-diabetic drugs, including sodium–glucose co-transporter 2 (SGLT2) inhibitors, dipeptidyl peptidase-4 (DPP-4) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, meglitinides, α-glucosidase inhibitors, thiazolidinediones, biguanides, insulin, and sulfonylureas.ResultsOne hundred seventeen eligible randomized controlled trials (RCTs) with 221,364 participants were included in this study. Compared with placebo, trelagliptin (RR 3.51; 1.58–13.70) increased the risk of fracture, whereas albiglutide (RR 0.29; 0.04–0.93) and voglibose (RR 0.03; 0–0.11) decreased the risk of fracture. Other medications were comparable in terms of their effects on fracture risk, and no statistical significance was observed. In terms of fractures, voglibose (0.01%) may be the safest option, and trelagliptin (13.64%) may be the worst. Sensitivity analysis results were consistent with those of the main analysis. No statistically significant differences were observed in the regression coefficients of age (1.03; 0.32–2.1), follow-up duration (0.79; 0.27–1.64), and sex distribution (0.63; 0.15–1.56).ConclusionsWe found varied results on the association between the use of anti-diabetic drugs and fracture risk. Specifically, trelagliptin raised the risk of fracture, whereas voglibose and albiglutide showed benefit with statistical difference. Other drugs were comparable in terms of their effects on fracture risk. Some drugs (omarigliptin, sitagliptin, vildagliptin, saxagliptin, empagliflozin, ertugliflozin, rosiglitazone, pioglitazone, and nateglinide) may increase the risk of fracture, while others (such as dulaglutide, exenatide, liraglutide, semaglutide, lixisenatide, linagliptin, alogliptin, canagliflozin, dapagliflozin, glipizide, gliclazide, glibenclamide, glimepiride, metformin, and insulin) may show benefits. The risk of fracture was independent of age, sex distribution, and the duration of exposure to anti-diabetic drugs. When developing individualized treatment strategies, the clinical efficacy of anti-diabetic drugs must be weighed against their benefits and risks brought about by individual differences of patients.Systematic Review RegistrationThis Systematic Review was prospectively registered on the PROSPERO (https://www.crd.york.ac.uk/PROSPERO/, registration number CRD42020189464).

Oxidative stress is considered as a major factor in aging and exacerbates aging process through a variety of molecular mechanisms. D-galactose, a normal reducing sugar with high dose can cause the accumulation of reactive oxygen species (ROS) or stimulate free radical production indirectly by the formation of advanced glycation end products in tissues, finally resulting in oxidative stress. 20(R)-ginsenoside Rg3 (20(R)-Rg3), a major and representative component isolated from red ginseng (Panax ginseng C.A Meyer), has been shown to observably have an anti-oxidative effect. We thereby investigated the beneficial effects of 20(R)-Rg3 on D-galactose-induced oxidative stress injury and its underlying mechanisms. Our results showed that continuous injection of D-galactose with 800[Formula: see text]mg/kg/day for 8 weeks increased the levels of alanine aminotransferase (ALT) and blood urea nitrogen (BUN). However, such increases were attenuated by the treatment of 20(R)-Rg3 for 4 weeks. Meanwhile, 20(R)-Rg3 markedly inhibited D-galactose-caused oxidative stress in liver and kidney. The anti-oxidants, including catalase (CAT) and superoxide dismutase (SOD), were elevated in the mice from 20(R)-Rg3-treated group compared with that from D-galactose group. In contrast, a significant decrease in levels of cytochrome P450 E1 (CYP2E1) and the lipid peroxidation product malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE) were observed in the 20(R)-Rg3-treated group. These effects were associated with a significant increase of AGEs. More importantly, 20(R)-Rg3 effectively attenuated D-galactose induced apoptosis in liver and kidney via restoring the upstream PI3K/AKT signaling pathway. Taken together, our study suggests that 20(R)-Rg3 may be a novel and promising anti-oxidative therapeutic agent to prevent aging-related injuries in liver and kidney.

Copper oxide (CuO) particles with loose agglomeration of porous flakes were treated by ultrasound in different solvents. CuO particles with completely discrete flakes were obtained with ultrasonic surface treatment in ethyl alcohol as a polar solvent while CuO particles with compacted flake agglomeration were found after ultrasonic treatment in diethyl ether as a non-polar solvent. CuO particles after ultrasonic treatment were characterized to investigate the effects of morphological appearance on size distribution, sedimentation velocity, specific surface area, ultraviolet-visible (UV–vis) absorption spectra, diffraction angle of X-ray diffraction (XRD) pattern, binding energy of X-ray photoelectron spectroscopy (XPS), Raman intensity and dissolution rate. CuO particles with completely discrete flakes exhibited a fastest dissolution rate of 7 s in 12.5 vol% H2SO4 for rapid complement of cupric ions so that the electrolyte for copper electrodepositon could meet the requirement of stable concentration of cupric ions to generate fine copper deposits in a plating system with insoluble anode.

Maltol, a maillard reaction product from ginseng (Panax ginseng C. A. Meyer), has been confirmed to inhibit oxidative stress in several animal models. Its beneficial effect on oxidative stress related brain aging is still unclear. In this study, the mouse model of d-galactose (d-Gal)-induced brain aging was employed to investigate the therapeutic effects and potential mechanisms of maltol. Maltol treatment significantly restored memory impairment in mice as determined by the Morris water maze tests. Long-term d-Gal treatment reduced expression of cholinergic regulators, i.e., the cholineacetyltransferase (ChAT) (0.456 ± 0.10 vs 0.211 ± 0.03 U/mg prot), the acetylcholinesterase (AChE) (36.4 ± 5.21 vs 66.5 ± 9.96 U/g). Maltol treatment prevented the reduction of ChAT and AChE in the hippocampus. Maltol decreased oxidative stress levels by reducing levels of reactive oxygen species (ROS) and malondialdehyde (MDA) production in the brain and by elevating antioxidative enzymes. Furthermore, maltol treatment minimized oxidative stress by increasing the phosphorylation levels of phosphatidylinositol-3-kinase (PI3K), protein kinase B (Akt), nuclear factor-erythroid 2-related factor 2 (Nrf2), and hemeoxygenase-1 (HO-1). The above results clearly indicate that supplementation of maltol diminishes d-Gal-induced behavioral dysfunction and neurological deficits via activation of the PI3K/Akt-mediated Nrf2/HO-1 signaling pathway in brain. Maltol might become a potential drug to slow the brain aging process and stimulate endogenous antioxidant defense capacity. This study provides the novel evidence that maltol may slow age-associated brain aging.

Successive evidence has established that maltol, a flavor-enhancing agent, could provide resistance to oxidative stress-induced tissue injury in various animal models though its benefits for aging-induced liver and kidney injuries are still undetermined. In the present work, for demonstrating maltol's ameliorative effect and probable mechanism against aging-induced liver and kidney injuries, D-galactose (D-Gal)-induced animal in vivo and HEK293 cells in vitro models were established and results demonstrated that long-term D-Gal treatment increases the accumulation of advanced glycation end products (AGEs) in liver and kidney tissues, mitigates cell viability, and arrests the cycle. Interestingly, 4-weeks maltol treatment at 50 and 100 mg/kg activated aging-associated proteins including p53, p21, and p16 followed by inhibiting malondialdehyde (MDA)'s over-production and increasing the levels of antioxidant enzymes. Therefore, decreases in cytochrome P450 E1 (CYP2E1) and 4-hydroxydecene (4-HNE)'s immunofluorescence expression levels are confirmed. Furthermore, maltol improved oxidative stress injury by activating the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. In conclusion, the purpose of the present study was to estimate the mechanistic insights into maltol's role as an antioxidant in liver and kidney cell senescence and injury, which will reflect potential of therapeutic strategy for antiaging and aging-related disease treatment.

Aims Subclinical lipohypertrophy is a lesion meeting ultrasonic criteria for lipohypertrophy that was not detected by inspection and palpation. Little information is published on subclinical lipohypertrophy among insulin injection people with diabetes. We aimed to investigate the subclinical lipohypertrophy prevalence, risk factors, and the association between subclinical lipohypertrophy and glycemic control. Methods This observational study included 316 people with diabetes who had continuously received insulin therapy for at least one year. We performed ultrasound scanning and clinical examination for evidence of subclinical lipohypertrophy. Demographic characteristics, clinical information, and glycated hemoglobin were measured. Results The overall prevalence of subclinical lipohypertrophy was 19.9%. By stepwise logistic regression, higher BMI (OR = 1.44, 95%CI: 1.15–1.81, P = 0.002), incorrect rotation of sites (OR = 3.11, 95%CI: 1.02–9.47, P = 0.046), insulin needle reusage for more than four times (OR = 10.00, 95%CI: 3.23–31.02, P = 0.000) and type 1 diabetes (OR = 6.33, 95%CI: 1.32–30.47, P = 0.021) remained associated with subclinical lipohypertrophy. Subclinical lipohypertrophy demonstrated a significant independent correlation with the nonoptimal glycemic control (OR = 9.97, 95% CI: 3.46–28.75, P = 0.000) when accounting for demographic and diabetes-related parameters. Conclusions Subclinical lipohypertrophy is common among insulin-injecting patients with diabetes and is related to glycemic control deterioration. Ultrasonography may be an ideal adjunct in the evaluation of easily ignored lipohypertrophy lesions, especially where poor glycemic control, incorrect injection behaviors, overweight or obesity are documented.

Cisplatin, as an effective chemotherapeutic agent, is widely used to treat verious types of cancers. Nephrotoxicity induced by cisplatin seriously limits its clinical application. Icariin, a major and remarkable flavonoid isolated from Epimedium koreanum, has been reported to exert anti-oxidative stress and anti-inflammation actions. The purpose of this study is to explore the protective effect and possible mechanism of icariin on cisplatin-induced nephrotoxicity on HEK-293 cells. In this study, icariin pretreatment for 24 h significantly ameliorated cisplatin-induced oxidative stress by reducing levels of malondialdehyde (MDA) and reactive oxygen species (ROS), while increasing level of glutathione (GSH) in HEK-293 cells. Furthermore, icariin pretreatment reduced NF-κB phosphorylation and nuclear translocation in HEK-293 cells followed by decreased secretion of IL-1β, TNF-α, and iNOS, suggesting a suppression of inflammatory response. Moreover, icariin pretreatment significantly reduced cellular apoptosis via reduced levels of Bax, cleaved caspase-3/9, and increased anti-apoptotic protein Bcl-2 in the cells. Importantly, LY294002, a specific PI3K inhibitor, abrogated the anti-apoptosis effect of icariin, implicating the involvement of PI3K/Akt pathway. In summary, icariin prevents cisplatin-induced HEK-293 cell injury by inhibiting oxidative stress, inflammatory response, and cellular apoptosis partly via regulating NF-κB and PI3K/Akt signaling pathways. Icariin may serve as a potential therapeutic target against cisplatin-induced nephrotoxicity.

Trans-arterial chemoembolization (TACE) has been a mainstream treatment for hepatocellular carcinoma (HCC), accordingly there are more requirements for embolic agents’ properties, mainly concentrated on biodegradability and imaging function. A new kind of biodegradable multifunctional porous microspheres (BMPMs) with internal coarse plications are ingeniously designed and manufactured, consisting of carrageenan, inhexol and superparamagnetic iron oxide nanoparticle (SPIO). BMPMs’ sound roundness and excellent swelling behavior guarantee them to be smoothly transported into appointed arteries’ ends and achieve satisfactory embolization effect. Porous structure together with sulphate groups on BMPMs’ skeleton weaved by cross-linked carrageenan contributes to a marvelous doxorubicin hydrochloride (Dox) loading capacity over 45 mg Dox per mL of swollen microspheres, as well as a controllable degradation rate by allowing enzymes to infiltrate into BMPMs through holes, degrading 20–35% after two months in vitro. Inner coarse plications enable BMPMs to effectively combine with iohexol via hydrophilic effect and SPIO by blocking, which can further exhibit a decent imaging performance under digital subtraction system (DSA) and magnetic resonance imaging (MRI) for optimization of current TACE and development of a more advanced imageable TACE (iTACE). Safety evaluation and animal experiment manifest that BMPMs are reliable enough and hold great potential and competitiveness of being used in curing HCC.

The miR-17~92 microRNA (miRNA) cluster host gene is upregulated in a broad spectrum of human cancers including colorectal cancer (CRC). Previous studies have shown that miR-17~92 promotes tumorigenesis and cancer angiogenesis in some tumor models. However, its role in the initiation and progression of CRC remains unknown. In this study, we found that transgenic mice overexpressing miR-17~92 specifically in epithelial cells of the small and large intestines exhibited decreased tumor size and tumor angiogenesis in azoxymethane and dextran sulfate sodium salt (AOM-DSS)-induced CRC model as compared to their littermates control. Further study showed that miR-17~92 inhibited the progression of CRC via suppressing tumor angiogenesis through targeting multiple tumor angiogenesis-inducing genes, TGFBR2, HIF1α, and VEGFA in vivo and in vitro. Collectively, we demonstrated that miR-17~92 suppressed tumor progression by inhibiting tumor angiogenesis in a genetically engineered mouse model, indicating the presence of cellular context-dependent pro- and anti-cancer effects of miR-17~92.

The purpose of this research was to evaluate whether maltol could protect from hepatic injury induced by carbon tetrachloride (CCl4) in vivo by inhibition of apoptosis and inflammatory responses. In this work, maltol was administered at a level of 100 mg/kg for 15 days prior to exposure to a single injection of CCl4 (0.25%, i.p.). The results clearly indicated that the intrapulmonary injection of CCl4 resulted in a sharp increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) activities, tumor necrosis factor-&alpha, (TNF-&alpha, ), irreducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-&kappa, B) and interleukin-1&beta, (IL-1&beta, ) levels. Histopathological examination demonstrated severe hepatocyte necrosis and the destruction of architecture in liver lesions. Immunohistochemical staining and western blot analysis suggested an accumulation of iNOS, NF-&kappa, B, IL-1&beta, and TNF-&alpha, expression. Maltol, when administered to mice for 15 days, can significantly improve these deleterious changes. In addition, TUNEL and Hoechst 33258 staining showed that a liver cell nucleus of a model group diffused uniform fluorescence following CCl4 injection. Maltol pretreatment groups did not show significant cell nuclear condensation and fragmentation, indicating that maltol inhibited CCl4-induced cell apoptosis. By evaluating the liver catalase (CAT), glutathione (GSH), superoxide dismutase (SOD) activity, and further using a single agent to evaluate the oxidative stress in CCl4-induced hepatotoxicity by immunofluorescence staining, maltol dramatically attenuated the reduction levels of hepatic CAT, GSH and SOD, and the over-expression levels of CYP2E1 and HO-1. In the mouse model of CCl4-induced liver injury, we have demonstrated that the inflammatory responses were inhibited, the serum levels of ALT and AST were reduced, cell apoptosis was suppressed, and liver injury caused by CCl4 was alleviated by maltol, demonstrating that maltol may be an efficient hepatoprotective agent.

Purpose To perform a quantitative analysis of retinal and choroid capillary ischaemia in diabetic patients by using optical coherence tomography angiography (OCTA). Methods A total of 97 type 2 diabetic patients and 48 controls were included in this cross-sectional study. Diabetic patients without diabetic retinopathy (DR) were categorized as no DR (NDR) group; DR was classified into mild non-proliferative diabetic retinopathy (NPDR), moderate NPDR, severe NPDR and proliferative diabetic retinopathy (PDR). Quantitative parameters included foveal and parafoveal vascular density (VD) in superficial, deep and choroid capillary plexus (SCP, DCP and CCP), and foveal flow area in CCP. Stepwise comparisons between groups were performed in the adjacent stages. Results Diabetic patients had significantly lower flow area in CCP and VD in all three layers compared with controls. In NDR group, foveal flow area in CCP significantly decreased compared with controls. In mild NPDR, parafoveal VD significantly decreased in all three layers compared with NDR, especially in temporal and nasal areas. In moderate NPDR, VD reduction extended to the inferior area in SCP and DCP compared with mild NPDR. In severe NPDR, progressive losses of VD were presented in all layers compared with moderate NDPR. In PDR, the superior VD in SCP significantly increased compared with severe NPDR. Conclusion In diabetic patients, the microvascular ischaemia originated in choroid layer and extended inward affecting the deep and superficial layer. OCTA can serve as a reliable method for early detection and to monitor progressions in diabetic retinopathy.

Examination of the retinal circulation in patients with retinal diseases is a clinical routine for ophthalmologists. In the present work, an automatic method is proposed for measuring the global retinal circulation in fluorescein angiography (FA). First, the perfusion region in FA images is segmented using a multiscale line detector. Then, the time evolution of the perfusion area is modeled using damped least-squares regression. Based on the perfusion area profile, some circulation parameters are defined to describe quantitatively the global retinal circulation. The effectiveness of the proposed method is tested using our own and public datasets, with reasonable results and satisfactory accuracy compared with manual measurement. The proposed method has good computing efficiency and thus has potential to be used in clinical practice for evaluation of global retinal circulation.

Rutin is one of the most common flavonoids present in nature that has a wide range of biological properties. A Tin(II)-rutin complex was synthesized from the raw material rutin and SnCl2 in an alkaline solution. The complex was characterized by UV-vis, IR, 1H NMR, and 13C NMR spectroscopy. We evaluated the free radical scavenging activity using the 1,1-diphenyl-2-picrylhydrazyl (DPPH) method, and the results showed that pure rutin was more effective than the Tin(II)-rutin complex in terms of antioxidant activity. Supplementing diet by foods rich in rutin and other flavonoids, such as vegetables and fruits, may contribute to removing free radicals and heavy metal ions in our body.

A novel complex, bis(trans-bis(N,N-dimethyl-(1-(R)-phenyl-2-(S)-methyl-2-aminoethoxy-N,O))-copper(II)) heptahydrate (abbreviated as Cu2(C11H16NO)4·7H2O(cr)), was synthesized by the method of liquid phase reflux. The composition and structure of the complex were characterized by chemical analysis, elemental analysis, FTIR, and X-ray crystallography. A reasonable thermochemical cycle was designed based on the preparation reaction of the coordination compound, and standard molar enthalpies of dissolution of reactants and products were measured by an isoperibol solution-reaction calorimeter. Finally, the standard molar enthalpy of formation of the complex Cu2(C11H16NO)4·7H2O(cr) was determined to be −(4525.22 ± 13.71) kJ · mol−1 in accordance with Hess’s law.

A coordination compound, ethylenediammonium tetrachlorocobaltate(II) chloride (H3NCH2CH2NH3)(2)[CoCl4]Cl-2, was synthesized by the method of liquid phase synthesis, in which ethylenediamine, cobalt chloride hexahydrate, and concentrated hydrochloric acid were chosen as the reactants. X-ray crystallography, chemical analysis, and elemental analysis were applied to characterize the structure and composition of the complex. Low-temperature heat capacities of the complex were measured with a precise automated adiabatic calorimeter over the temperature range from (78 to 370) K. A polynomial equation of the heat capacities as a function of temperature was fitted by a least-squares method. Smoothed heat capacities and thermodynamic functions of the compound relative to the standard reference temperature of 298.15 K were calculated and tabulated at intervals of 5 K based on the fitted polynomial equation. A reasonable thermochemical cycle was designed, and the standard molar enthalpies of dissolution of the reactants and products of the synthesis reaction in the selected solvent were measured by an isoperibol solution-reaction calorimeter. The enthalpy change of the reaction was calculated to be Delta H-r(m)o = (17.612 +/- 0.571) kJ.mol(-1) from the data of the standard molar enthalpies of dissolution. The standard molar enthalpy of formation of the title compund was determined to be Delta H-f(m)o {(NH3CH2CH2NH3)(2)[CoCl4]Cl-2, s} = (1499.54 +/- 2.73) kJ.mol(-1) in accordance with Hess's law.

Ethylenediamine dihydrochloride (C 2 H 10 N 2 Cl 2 )(s) was synthesized. The crystal structure of the compound has been determined by X-ray crystallography. The lattice potential energy and ionic radius of the cation of the compound were obtained from the crystallographic data. Molar enthalpies of dissolution of the compound in double-distilled water under various values of molality were determined at T = 298.15 K by an isoperibol solution-reaction calorimeter. Following to Pitzer’s theory, the molar enthalpy of dissolution of the compound at infinite dilution ( Δ sol H m ∞ ) and the Pitzer parameters ( β MX ( 0 ) L and β MX ( 1 ) L ) were obtained. The values of relative apparent molar enthalpies ( Φ L ), relative partial molar enthalpies ( L ¯ 2 ) of the compound and relative partial molar enthalpies ( L ¯ 1 ) of the solvent at different concentrations m /(mol · kg −1 ) were derived from the experimental values of the enthalpies of dissolution of the compound. Finally, the hydration enthalpy of the cation of the substance was calculated by designing a thermochemical cycle.

Substrate selectivity of glycerol-3-phosphate acyltransferase (EC 2. 3. 1. 15) of rice (Oryza sativa L.) was explored in a comparative study of acyltransferases from seven plant species. In vitro labeling of acyl carrier protein (ACP) with (14)C or (3)H showed that acyltransferase from chill-sensitive plants, such as rice that uses either oleic (18:1) or palmitic acid (16:0) as acyl donor at comparable rates, displays lower selectivity than the enzyme from chill-resistant plants, such as spinach, which preferentially uses oleic acid (18:1) rather than palmitic acid (16:0) as an acyl donor. This may be a result of the size and character of the substrate-binding pocket of acyltransferase. Homology modeling and protein structure-based sequence alignment of acyltransferases revealed that proteins from either chill-sensitive or chill-tolerant plants shared a highly conserved domain containing the proposed substrate-binding pocket. However, the aligned residues surrounding the substrate-binding pocket are highly heterogeneous and may have an influence mainly on the size of the substrate binding pockets of acyltransferases. The substrate selectivity of acyltransferase of rice can be improved by enlarging the substrate-binding pocket using molecular biological methods.

Nanoscaled zinc oxide (ZnO) particles with different amounts are coated on titanate nanotubes (TNTs) by a facile chemical method at room temperature. The characterizations of XPS, TEM, XRD and UV–vis spectra confirm that pure hexagonal wurtzite ZnO nanoparticles with an average size of about 9 nm are distributed on the surfaces of TNTs evenly and attached strongly. The photocatalytic activities of the ZnO–TNTs nanocomposite are superior to those of P25, ZnO, TNTs and ZnO–anatase TiO 2 (TNP) nanocomposite in the oxidation of rhodamine B under UV light irradiation. A comparison of the photocatalytic activities between different catalysts is discussed. Furthermore, we also find that the ZnO–TNT nanocomposite shows very favorable recycle use potential, because they have a high sedimentation rate and their photocatalytic activity is only slightly decreased even after five times of repeated uses.

Background/aims To investigate the effect of mycophenolate mofetil (MMF) on acute liver injury induced by bacille Calmette-Guerin (BCG) and lipopolysaccharide (LPS). Methods Acute liver failure was induced in male Kunming strain mice by injecting the animals with BCG 2.5 mg per mouse, and LPS 10 microg per mouse 10 days later. The mice in the treatment groups were given MMF 2 h before, simultaneous with, or 2 h after administration of LPS, and the mice in the control group were given the same dose of saline. The 24-h survival rate, serum alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were compared. Serum levels of tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), and interleukin 6 (IL-6) were measured and the expressions of TNF-alpha, IFN-gamma, and IL-6 mRNA in the liver tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR). Concanavalin A (Con A)-induced splenocyte proliferation were determined by methods of methyl thiazolyl tetrazolium. Results Injecting a small dose of LPS into BCG-primed mice caused a lethal hepatic injury mimicking acute hepatitis, from which 16 of the 20 mice died within 24 h (20% survival rate). Massive necrosis of parenchymal hepatocytes with marked inflammatory cell infiltration was observed by histological examination. In parallel, serum ALT and TNF-alpha, IFN-gamma, and IL-6 levels were increased. Expression of TNF-alpha, IFN-gamma, and IL-6 mRNA in the liver were significantly increased also. Treatment with MMF markedly reduced the death rate in a dose-dependent manner. It reached its maximal effect at the dosage of 150 mg per kg of body weight when pretreated 2 h before LPS injection, with improvement of histological feather and survival rate (84.2%, 16/19). MMF significantly inhibited serum levels of TNF-alpha, IFN-gamma, and IL-6, and significantly reduced TNF-alpha, IFN-gamma, and IL-6 expression in the liver, which increased after BCG and LPS injection. Moreover, splenocyte proliferation response induced by Con A was also inhibited by MMF treatment. Conclusions Treatment with MMF has a protective effect on endotoxin-induced fatal liver failure by regulating the production of inflammatory cytokines and T-cell proliferation.

In the present work, we investigated the effect of ascorbic acid and glutathione on hemolysis induced by hemin in erythrocytes. Ascorbic acid not only enhanced hemolysis, but also induced formation of thiobarbituric acid-reactive substances in the presence of hemin. It has been shown that glutathione inhibits hemin-induced hemolysis by mediating hemin degradation. Erythrocytes depleted of glutathione became very sensitive to oxidative stress induced by hemin and ascorbic acid. H(2)O(2) was involved in hemin-mediated hemolysis in the presence of ascorbic acid. However, a combination of glutathione and ascorbic acid was more effective in inhibiting hemolysis induced by hemin than glutathione alone. Extracellular and intracellular ascorbic acid exhibited a similar effect on hemin-induced hemolysis or inhibition of hemin-induced hemolysis by glutathione. The current study indicates that ascorbic acid might function as an antioxidant or prooxidant in hemin-mediated hemolysis, depending on whether glutathione is available.

Quercetin-germanium (Ge) (IV) complex was synthesized in the laboratory. The structure and physicochemical properties of the complex were characterized utilizing thermal and spectroscopic (UV-vis, IR and 1H NMR) analysis. The antitumor activity of quercetin-Ge (IV) compound was evaluated by the MTT method. The complex was subjected to biological tests in vitro using four tumor cell lines (PC-3, Hela, EC9706 and SPC-A-1). The quercetin-Ge (IV) complex showed significant cytotoxicity against four tumor cell lines.

Nanoscopic CdS particles are decorated into the microchannel with nanometre-scale diameter of titanate nanotubes (TNTs) by using nonionic thioacetamide (TAA) as a sulfide precursor (labelled as CdS(TAA)/TNTs). The characterizations by XPS, TEM, XRD, Raman spectroscopy and UV-vis absorption confirm that CdS nanoparticles with smaller size and more homogeneous dispersion are obtained by using a TAA precursor in contrast to the particles predominantly formed on the surface of TNTs by adding ionic Na(2)S as a precursor (labelled as CdS(Na(2)S)/TNTs). As is expected, the photocatalytic activities of the nanosized CdS sensitized TNTs nanocrystal materials were superior to those of simple CdS and TNTs in the oxidation of rhodamine B under visible light irradiation. Furthermore, the comparison of photocatalysis activity between CdS(TAA)/TNTs and CdS(Na(2)S)/TNTs is also discussed.

In the crystal of the title compound, C(15)H(34)N(+)center dot CH(3)SO(4)(-), the cations and anions are joined together via strong N-H center dot center dot center dot O hydrogen bonds into layers parallel to (001).

In the title compound, C12H28N+·Br−·H2O, the ionic pairs formed by n-dodecylammonium cations and bromide anions are arranged into thick layers; these layers are linked in a nearly perpendicular fashion [the angle between the layers is 85.84 (5)°] by hydrogen-bonding interactions involving the water molecules. The methylene part of the alkyl chain in the cation adopts an all-trans conformation. In the crystal structure, molecules are linked by intermolecular N—H...Br, O—H...Br and N—H...O hydrogen bonds.

The feasibility of transforming embryonic endoderm into different cell types is tightly controlled by mesodermal and septum transversumal signalings during early embryonic development. Here, an induction protocol tracing embryonic liver development was designed, in which, three growth factors, acid fibroblast growth factor, basic fibroblast growth factor and bone morphological protein-4 that secreted from pre-cardiac mesoderm and septum transversum mesenchyme, respectively, were employed to investigate their specific potency of modulating the mature hepatocyte proportion during the differentiation process. Results showed that hepatic differentiation took place spontaneously at a low level, however, supplements of the three growth factors gave rise to a significant up-regulation of mature hepatocytes. Bone morphological protein-4 highlighted the differentiation ratio to 40-55%, showing the most effective promotion, and also exhibited a synergistic effect with the other two fibroblast factors, whereas no similar phenomenon was observed between the other two factors, which was reported for the first time. Our study not only provides a high-performance system of embryonic stem cells differentiating into hepatocytes, which would supply a sufficient hepatic population for related studies, but also make it clear of the inductive effects of three important growth factors, which could support for further investigation on the mechanisms of mesodermal and septumal derived signalings that regulate hepatic differentiation.

Reaction of Pt(diimine)(edt) (edt = 1,2-ethanedithiolate) with M(2)(dppm)(2)(MeCN)(2)(2+) (dppm = bis(diphenylphosphino)methane) gave heterotrinuclear complexes [PtCu(2)(edt)(mu-SH)(dppm)(3)](ClO(4)) (11) and [PtCu(2)(diimine)(2)(edt)(dppm)(2)](ClO(4))(2) (diimine = 2,2'-bpyridine (bpy), 12; 4,4'-dibutyl-2,2'-bipyridine (dbbpy), 13; phenanthroline (phen), 14; 5-bromophenanthroline (brphen), 15) when M = Cu(I). The reaction, however, afforded tetra- and trinuclear complexes [Pt(2)Ag(2)(edt)(2)(dppm)(2)](SbF(6))(2) (17) and [PtAu(2)(edt)(dppm)(2)](SbF(6))(2) (21) when M = Ag(I) and Au(I), respectively. The complexes were characterized by elemental analyses, electrospray mass spectroscopy, (1)H and (31)P NMR, IR, and UV-vis spectrometry, and X-ray crystallography for 14, 17, and 18. The Pt(II)Cu(I)(2) heterotrinuclear complexes 11-15 exhibit photoluminescence in the solid states at 298 K and in the frozen acetonitrile glasses at 77 K. It is likely that the emission originates from a ligand-to-metal charge transfer (dithiolate-to-Pt) (3)[p(S) --d(Pt)] transition for 11 and from an admixture of (3)[d(Cu)/p(S)-pi(diimine)] transitions for 12-16. The Pt(II)(2)Ag(I)(2) heterotetranuclear complexes 17 and 18 are nonemissive in the solid states and in solutions at 298 K but show photoluminescence at 77 K. The Pt(II)Au(I)(2) heterotrinuclear complexes 19-21, however, are luminescent at room temperature in the solid state and in solution. Compounds 19 and 20 afford negative solvatochromism associated with a charge transfer from an orbital of a mixed metal/dithiolate character to a diimine pi orbital.

Reactions of Pt(diimine)(tdt) (tdt =3,4-toluenedithiolate) with [M(2)(dppm)(2)(MeCN)(2)](2+) (M = Cu(I) or Ag(I), dppm = bis(diphenylphosphino)methane) gave heterotrinuclear complexes [PtCu(2)(tdt)(mu-SH)(dppm)(3)](ClO(4)) (1) and [PtCu(2)(diimine)(2)(tdt)(dppm)(2)](ClO(4))(2) (diimine = 2,2'-bpyridine (bpy) 2; 4,4'-dimethyl-2,2'-bipyridine (dmbpy) 3; phenanthroline (phen) 4, 5-bromophenanthroline (Brphen) 5) for M = Cu(I), but [PtAg(2)(tdt)(mu-SH)(dppm)(3)](SbF(6)) (6) and [PtAg(2)(diimine)(tdt)(dppm)(2)](SbF(6))(2) (diimine = bpy 7; dmbpy 8; phen 9; Brphen 10) for M = Ag(I). While the complexes [PtAg(2)(diimine)(tdt)(dppm)(2)](SbF(6))(2) (7-10) result from linkage of Pt(diimine)(tdt) and [M(2)(dppm)(2)(MeCN)(2)](2+) by tdt sulfur donors, formation of [PtCu(2)(diimine)(2)(tdt)(dppm)(2)](ClO(4))(2) (2-5) is related to rupture of metal-ligand bonds in the metal components and recombination between the ligands and the metal atoms by self-assembly. The formation of 1 and 6 is involved not only in dissociation and recombination of the metal components, but also in disruption of C-S bonds in the dithiolate (tdt). The dithiolate tdt adopts a chelating and bridging coordination mode in anti conformation for [PtCu(2)(diimine)(2)(tdt)(dppm)(2)](ClO(4))(2) (2-5), whereas there is the syn conformation for other complexes. Compounds 1 and 6 represent sparse examples of mu-SH-bridged heterotrinuclear Pt(II)M(I)(2) complexes, in which Pt(II)-M(I) centers are bridged by dppm and sulfur donors of tdt, whereas M(I)-M(I) (M = Cu for 1; Ag for 6) centers are linked by dppm and the mu-SH donor. The (31)P NMR spectra show typical platinum satellites (J(Pt-P) = 1450-1570 Hz) for 1-6 and Ag-P coupling for Pt(II)-Ag(I) (J(Ag-P) = 350-450 Hz) complexes 6-10. All of the complexes show intense emission in the solid state and in frozen glasses at 77 K. The complexes [PtAg(2)(diimine)(tdt)(dppm)(2)](SbF(6))(2) (7-10) also afford emission in fluid acetonitrile solutions at room temperature. Solid-state emission lifetimes at room temperature are in the microsecond range. It is revealed that emission energies of the trinuclear heterometallic complexes [PtAg(2)(diimine)(tdt)(dppm)(2)](SbF(6))(2) (7-10) exhibit a remarkable blue shift (0.10-0.35 eV) relative to those of the precursor compounds Pt(diimine)(tdt). The crystal structures of 1, 2, 4, 6, 8, and 9 were determined by X-ray crystallography.

The title compound, [Re(C2H3N)(C10H8N2)(CO)3]ClO4, was isolated from the reaction between [ReCl(bpy)(CO)3] (bpy is 2,2′-bipyridine) and AgClO4 in acetonitrile. The Re atom adopts a distorted octahedral geometry.

[Re(C2H3N)(C10H8N2)2(CO)3][SbF6]·0.5CH2Cl2 was isolated from the reaction between [Re(bpy)(CO)3Cl], where bpy = 2,2'-bipyridine, and AgSbF6 in aceto­nitrile. The rhenium atom has a distorted octahedral geometry.

The title binuclear ReI–thiol­ate complex, [Re2(C6H5S)(C10H8N2)2(CO)6]ClO4·0.5CH2Cl2, was isolated from the reaction between [Re(bpy)(CO)3](SC6H5) and [Cu2(μ2-dppm)2(MeCN)4](ClO4)2 (bpy is bi­pyridine and dppm is di­phenyl­phosphino­methane). The two rhenium–di­imine moieties are bridged by one S-donor and each Re atom adopts a distorted octahedral geometry.