Programmable multimode optical encryption of advanced printable security inks by integrating structural color with Down/Up- conversion photoluminescence.

Optical information encryption with high encoding capacities can significantly boost the security level of anti-counterfeiting in the scenario of guaranteeing the authenticity of a wide scope of common and luxury goods. In this work, a novel counterfeiting material with high-degree complexity is fabricated by microencapsulating cholesteric liquid crystals and triplet-triplet annihilation upconversion fluorophores to integrate structural coloration with fluorescence and upconversion photoluminescence. Moreover, the multimode security ink presents tailorable optical behaviors and programmable abilities on flexible substrates by various printing techniques, which offers distinct information encryption under different optical modes. The advanced strategy provides a practical versatile platform for high-secure-level multimode optical inks with largely enhanced encoding capacities, programmability, printability, and cost-effectiveness, which manifests enormous potentials for information encryption and anti-counterfeiting technology.

Preparation and Orthogonal Analysis for Dual-Responsive Electrochromic Polymer Dispersed Liquid Crystal Devices.

In this work, we provide a fabrication method for dual-responsive electrochromic (EC) polymer dispersed liquid crystal (PDLC) devices. The EC PDLC device was developed by combing the PDLC technique and a colored complex formed via a redox reaction without a specific EC molecule in a simple preparation method. The mesogen played dual roles in the device for scattering in the form of microdroplets and participating in the redox reactions. Orthogonal experiments were performed with the acrylate monomer concentration, the ionic salt concentration, and the cell thickness as factors to investigate the electro-optical performance for the achievement of optimized fabrication conditions. The optimized device presented four switchable states modulated by external electric fields. The light transmittance of the device was changed by an alternative current (AC) electric field while the color change was realized by a direct current (DC) electric field. Variations of mesogen and ionic salt species can modulate the color and hue of devices, which solves the disadvantage of a single color for traditional EC devices. This work lays the foundation for realizing patterned multi-colored patterned displays and anti-counterfeiting via screen printing and inkjet printing techniques.

Ratiometric Fluorescence Detection of Mg2+ Based on Regulating Crown-Ether Modified Annihilators for Triplet-Triplet Annihilation Upconversion.

Detection of magnesium ion has been of great significance considering its critical physiological activities. Herein, we report ratiometric fluorescence detection of Mg2+ with high sensitivity and selectivity based on triplet-triplet annihilation (TTA) upconversion for the first time. Crown-ether functionalized anthracene derivatives were synthesized, which bifunctionally acted as not only annihilators to construct TTA upconversion systems but also the recognition probes for Mg2+ based on the photoinduced electron transfer (PET) mechanism. Their photophysical properties with the absence and presence of Mg2+ were comprehensively studied. It was found that solvents strongly influenced the photophysical properties and Mg2+-responsiveness. TTA upconversion systems with PtOEP as the sensitizer were further established and investigated. It turned out PtOEP/9-AEC in DCM exhibited an excellent linear relationship (R2 = 0.9979) between the intensity ratio (the integrated upconverted luminescence intensity (IUC) over the integrated downshifted phosphorescence intensity (IPL), IUC/IPL) and the concentration of Mg2+ under the excitation of 532 nm with a limit of detection value of 2.52 µM and a high selectivity to Mg2+. This work opened a new perspective of designs and applications of TTA-upconversion-based ratiometric fluorescence for ion detection.

In vitro performance of 3D printed PCL-ß-TCP degradable spinal fusion cage.

Spinal fusion cages are commonly used to treat spinal diseases caused by degenerative changes, deformities, and trauma. At present, most of the main clinical spinal fusion cage products are non-degradable and still cause some undesirable side effects, such as the stress shielding phenomenon, interference with postoperative medical imaging, and obvious foreign body sensation in patients. Degradable spinal fusion cages have promising potential with extensive perspectives. The purpose of this study was to fabricate a degradable spinal fusion cage from both polycaprolactone (PCL) and high-proportion beta-tricalcium phosphate (ß-TCP), using the highly personalised, accurate, and rapid fused deposition modelling 3 D printing technology. PCL and ß-TCP were mixed in three different ratios (60:40, 55:45, and 50:50). Both in vitro degradation and cell experiments proved that all cages with the different PCL:ß-TCP ratios met the mechanical properties of human cancellous bone while maintaining their structural integrity. The biological activity of the cages improved with higher amounts of the ß-TCP content. This study also showed that a spinal fusion cage with high ß-TCP content and suitable mechanical properties can be manufactured using extruding rods and appropriate models, providing a new solution for the design of degradable spinal fusion cages.

An Injectable Nanocomposite Hydrogel for Potential Application of Vascularization and Tissue Repair.

In this contribution, an injectable hydrogel was developed with chitosan, gelatin, ß-glycerphosphate and Arg-Gly-Asp (RGD) peptide: this hydrogel is liquid in room temperature and rapidly gels at 37 °C; RGD peptide promises better growth microenvironment for various cells, especially endothelial cells (EC), smooth muscle cells (SMC) and mesenchymal stem cells (MSC). Both stromal cell-derived factor-1 (SDF-1) nanoparticle and vascular endothelial growth factor (VEGF) nanoparticles were loaded in the injectable hydrogel to simulate the natural nanoparticles in the extracellular matrix (ECM) to promote angiogenesis. In vitro EC/SMC and MSC/SMC co-culture experiment indicated that the nanocomposite hydrogel accelerated constructing embryonic form of blood vessels, and chick embryo chorioallantoic membrane model demonstrated its ability of improving cells migration and blood vessel regeneration. We injected this nanocomposite hydrogel into rat myocardial infarction (MI) model and the results indicated that the rats heart function recovered better compared control group. We hope this injectable nanocomposite hydrogel may possess wider application in tissue engineering.

Deficiency of Invariant Natural Killer T Cells Does Not Protect Against Obesity but Exacerbates Atherosclerosis in Ldlr-/- Mice.

Obesity is a chronic inflammatory state characterized by altered levels of adipose tissue immune cell populations. Natural killer T (NKT) cells are CD1d restricted lymphocyte subsets that recognize lipid antigens whose level decreases in obese adipose tissue. However, studies in mice with deficiency or increased levels of NKT cells have yielded contradictory results, so the exact role of these cells in obesity and adipose tissue inflammation is not yet established. We previously showed that Ldlr-/- mice with excess invariant NKT (iNKT) cells demonstrate significant weight gain, adiposity, metabolic abnormalities, and atherosclerosis. The current study evaluates the effects of NKT cell deficiency on obesity, associated metabolic changes, and atherosclerosis in Jα18-/-Ldlr-/- (lacking iNKT cells) and Cd1d-/-Ldlr-/- (lacking invariant and type II NKT cells) mice, and control mice were fed an obesogenic diet (high fat, sucrose, cholesterol) for 16 weeks. Contrary to expectations, Ja18-/-Ldlr-/- mice gained significantly more weight than Ldlr-/- or Cd1d-/-Ldlr-/- mice, developed hypertriglyceridemia, and had worsened adipose tissue inflammation. All the mice developed insulin resistance and hepatic triglyceride accumulation. Ja18-/-Ldlr-/- mice also had increased atherosclerotic lesion area. Our findings suggest that iNKT cells exacerbates the metabolic, inflammatory, and atherosclerotic features of diet-induced obesity. Further work is required to unravel the paradox of an apparently similar effect of iNKT cell surplus and depletion on obesity.

Income related inequality and influencing factors: a study for the incidence of catastrophic health expenditure in rural China.

BACKGROUND: Catastrophic health expenditure (CHE) puts a heavy disease burden on patients' families, aggravating income-related inequality. In an attempt to reduce the financial risks of rural families incurring CHE, China began the New Rural Cooperative Medical System (NCMS) on a trial basis in 2003 and has raised the reimbursement rates continuously since then. Based on statistical data about rural families in sample area of Jiangsu province, this study measures the incidence of CHE, analyzes socioeconomic inequality related to CHE, and explores the influences of the NCMS on the incidence of CHE. METHODS: Statistical data were acquired from two surveys about rural health care, one conducted in 2009 and one conducted in 2010. In 2009, 1424 rural families were analyzed; in 2010, 1796 rural families were analyzed. An index of CHE is created to enable the evaluation of the associated financial risks. The concentration index and concentration curve are used to measure the income-related inequality involved in CHE. Multiple logistic regression is utilized to explore the factors that influence the incidence of CHE. RESULTS: The incidence of CHE decreased from 13.62% in 2009 to 7.74% in 2010. The concentration index of CHE was changed from -0.298 (2009) to -0.323 (2010). Compared with rural families in which all members were covered by the NCMS, rural families in which some members were not covered by the NCMS had a lower incidence of CHE: The odds ratio is 0.65 with a 95% confidence interval of 0.43 to 1.00. For rural families in which all members were covered by the NCMS, the increase in reimbursement rates is correlated to the decline in the incidence of CHE if other influencing factors were controlled: The odds ratio is 0.48 with a 95% confidence interval of 0.36 to 0.64. CONCLUSIONS: Between 2009 and 2010, the incidence rate of CHE in the sampled area decreased sharply, CHE was more concentrated among least wealthy and inequality increased during study period. As of 2010, the poorest rural families still had high risk of experiencing CHE. For rural families in which all members are covered by the NCMS, the rise in reimbursement rates reduces the probability of experiencing CHE.

Correlation Between New Cooperative Medical Scheme Policy Design and Catastrophic Medical Payment: Evidence From 25 Counties in Rural China.

Few studies have examined the association between the New Cooperative Medical Scheme (NCMS) policy design and its achievement of providing financial protection to rural residents. This study collected data on NCMS policy design and health care spending from 25 counties and rural households in their catchment areas. It shows that on average, NCMS has a growing but small effect on the reduction of catastrophic medical payment (CMP) incidence. If outpatient spending can be reimbursed from an NCMS pooled account, the incidence of CMP before a reimbursement and that after a reimbursement will be reduced. Higher nominal reimbursement rate for inpatient spending at provincial hospitals is correlated with higher incidence of CMP before a reimbursement. Higher ceiling for annual reimbursement from NCMS is associated with lower incidence of CMP after a reimbursement. Thus, NCMS policy design can be improved to strengthen its effects on the reduction of CMP incidence.

The apolipoprotein-AI mimetic peptide L4F at a modest dose does not attenuate weight gain, inflammation, or atherosclerosis in LDLR-null mice.

OBJECTIVE: High density lipoprotein (HDL) cholesterol levels are inversely related to cardiovascular disease risk and associated with a reduced risk of type 2 diabetes. Apolipoprotein A-I (apoA-I; major HDL protein) mimetics have been reported to reduce atherosclerosis and decrease adiposity. This study investigated the effect of L4F mimetic peptide and apoA-I overexpression on weight gain, insulin resistance, and atherosclerosis in an LDL receptor deficient (Ldlr-/-) model fed a high fat high sucrose with cholesterol (HFHSC) diet. METHODS: Studies in differentiated 3T3-L1 adipocytes tested whether L4F could inhibit palmitate-induced adipocyte inflammation. In vivo studies used male Ldlr-/- mice fed a HFHSC diet for 12 weeks and were injected daily with L4F (100 µg/mouse) subcutaneously during the last 8 weeks. Wild-type and apoA-I overexpressing Ldlr-/- mice were fed HFHSC diet for 16 weeks. RESULTS: Neither L4F administration nor apoA-I overexpression affected weight gain, total plasma cholesterol or triglycerides in our studies. While pre-treatment of 3T3-L1 adipocytes with either L4F or HDL abolished palmitate-induced cytokine expression in vitro, L4F treatment did not affect circulating or adipose tissue inflammatory markers in vivo. Neither L4F administration nor apoA-I overexpression affected glucose tolerance. ApoA-I overexpression significantly reduced atherosclerotic lesion size, yet L4F treatment did not affect atherosclerosis. CONCLUSION: Our results suggest that neither L4F (100 µg/day/mouse) nor apoA-I overexpression affects adiposity or insulin resistance in this model. We also were unable to confirm a reduction in atherosclerosis with L4F in our particular model. Further studies on the effect of apoA-I mimetics on atherosclerosis and insulin resistance in a variety of dietary contexts are warranted.

Deletion of serum amyloid A3 improves high fat high sucrose diet-induced adipose tissue inflammation and hyperlipidemia in female mice.

Serum amyloid A (SAA) increases in response to acute inflammatory stimuli and is modestly and chronically elevated in obesity. SAA3, an inducible form of SAA, is highly expressed in adipose tissue in obese mice where it promotes monocyte chemotaxis, providing a mechanism for the macrophage accumulation that occurs with adipose tissue expansion in obesity. Humans do not express functional SAA3 protein, but instead express SAA1 and SAA2 in hepatic as well as extrahepatic tissues, making it difficult to distinguish between liver and adipose tissue-specific SAA effects. SAA3 does not circulate in plasma, but may exert local effects that impact systemic inflammation. We tested the hypothesis that SAA3 contributes to chronic systemic inflammation and adipose tissue macrophage accumulation in obesity using mice deficient for Saa3 (Saa3(-/-)). Mice were rendered obese by feeding a pro-inflammatory high fat, high sucrose diet with added cholesterol (HFHSC). Both male and female Saa3(-/-) mice gained less weight on the HFHSC diet compared to Saa3(+/+) littermate controls, with no differences in body composition or resting metabolism. Female Saa3(-/-) mice, but not males, had reduced HFHSC diet-induced adipose tissue inflammation and macrophage content. Both male and female Saa3(-/-) mice had reduced liver Saa1 and Saa2 expression in association with reduced plasma SAA. Additionally, female Saa3(-/-) mice, but not males, showed improved plasma cholesterol, triglycerides, and lipoprotein profiles, with no changes in glucose metabolism. Taken together, these results suggest that the absence of Saa3 attenuates liver-specific SAA (i.e., SAA1/2) secretion into plasma and blunts weight gain induced by an obesogenic diet. Furthermore, adipose tissue-specific inflammation and macrophage accumulation are attenuated in female Saa3(-/-) mice, suggesting a novel sexually dimorphic role for this protein. These results also suggest that Saa3 influences liver-specific SAA1/2 expression, and that SAA3 could play a larger role in the acute phase response than previously thought.

Increased levels of invariant natural killer T lymphocytes worsen metabolic abnormalities and atherosclerosis in obese mice.

Obesity is a chronic inflammatory state characterized by infiltration of adipose tissue by immune cell populations, including T lymphocytes. Natural killer T (NKT) cells, a specialized lymphocyte subset recognizing lipid antigens, can be pro- or anti-inflammatory. Their role in adipose inflammation continues to be inconclusive and contradictory. In obesity, the infiltration of tissues by invariant NKT (iNKT) cells is decreased. We therefore hypothesized that an excess iNKT cell complement might improve metabolic abnormalities in obesity. Vα14 transgenic (Vα14tg) mice, with increased iNKT cell numbers, on a LDL receptor-deficient (Ldlr(-/-)) background and control Ldlr(-/-) mice were placed on an obesogenic diet for 16 weeks. Vα14tg.Ldlr(-/-) mice gained 25% more weight and had increased adiposity than littermate controls. Transgenic mice also developed greater dyslipidemia, hyperinsulinemia, insulin resistance, and hepatic triglyceride accumulation. Increased macrophage Mac2 immunostaining and proinflammatory macrophage gene expression suggested worsened adipose inflammation. Concurrently, these mice had increased atherosclerotic lesion area and aortic inflammation. Thus, increasing the complement of iNKT cells surprisingly exacerbated the metabolic, inflammatory, and atherosclerotic features of obesity. These findings suggest that the reduction of iNKT cells normally observed in obesity may represent a physiological attempt to compensate for this inflammatory condition.

T cell activation inhibitors reduce CD8+ T cell and pro-inflammatory macrophage accumulation in adipose tissue of obese mice.

Adipose tissue inflammation and specifically, pro-inflammatory macrophages are believed to contribute to insulin resistance (IR) in obesity in humans and animal models. Recent studies have invoked T cells in the recruitment of pro-inflammatory macrophages and the development of IR. To test the role of the T cell response in adipose tissue of mice fed an obesogenic diet, we used two agents (CTLA-4 Ig and anti-CD40L antibody) that block co-stimulation, which is essential for full T cell activation. C57BL/6 mice were fed an obesogenic diet for 16 weeks, and concomitantly either treated with CTLA-4 Ig, anti-CD40L antibody or an IgG control (300 µg/week). The treatments altered the immune cell composition of adipose tissue in obese mice. Treated mice demonstrated a marked reduction in pro-inflammatory adipose tissue macrophages and activated CD8+ T cells. Mice treated with anti-CD40L exhibited reduced weight gain, which was accompanied by a trend toward improved IR. CTLA-4 Ig treatment, however, was not associated with improved IR. These data suggest that the presence of pro-inflammatory T cells and macrophages can be altered with co-stimulatory inhibitors, but may not be a significant contributor to the whole body IR phenotype.

Inhibition of intestinal cholesterol absorption decreases atherosclerosis but not adipose tissue inflammation.

Adipose tissue inflammation is associated with insulin resistance and increased cardiovascular disease risk in obesity. We previously showed that addition of cholesterol to a diet rich in saturated fat and refined carbohydrate significantly worsens dyslipidemia, insulin resistance, adipose tissue macrophage accumulation, systemic inflammation, and atherosclerosis in LDL receptor-deficient (Ldlr(-/-)) mice. To test whether inhibition of intestinal cholesterol absorption would improve metabolic abnormalities and adipose tissue inflammation in obesity, we administered ezetimibe, a dietary and endogenous cholesterol absorption inhibitor, to Ldlr(-/-) mice fed chow or high-fat, high-sucrose (HFHS) diets without or with 0.15% cholesterol (HFHS+C). Ezetimibe blunted weight gain and markedly reduced plasma lipids in the HFHS+C group. Ezetimibe had no effect on glucose homeostasis or visceral adipose tissue macrophage gene expression in the HFHS+C fed mice, although circulating inflammatory markers serum amyloid A (SSA) and serum amyloid P (SSP) levels decreased. Nevertheless, ezetimibe treatment led to a striking (>85%) reduction in atherosclerotic lesion area with reduced lesion lipid and macrophage content in the HFHS+C group. Thus, in the presence of dietary cholesterol, ezetimibe did not improve adipose tissue inflammation in obese Ldlr(-/-) mice, but it led to a major reduction in atherosclerotic lesions associated with improved plasma lipids and lipoproteins.

Toll-like receptor 4 deficiency decreases atherosclerosis but does not protect against inflammation in obese low-density lipoprotein receptor-deficient mice.

OBJECTIVE: Obesity is associated with insulin resistance, chronic low-grade inflammation, and atherosclerosis. Toll-like receptor 4 (TLR4) participates in the cross talk between inflammation and insulin resistance, being activated by both lipopolysaccharide and saturated fatty acids. The present study was undertaken to determine whether TLR4 deficiency has a protective role in inflammation, insulin resistance, and atherosclerosis induced by a diabetogenic diet. METHODS AND RESULTS: TLR4 and low-density lipoprotein (LDL) receptor double knockout mice and LDL receptor-deficient mice were fed either a normal chow or a diabetogenic diet for 24 weeks. TLR4 and LDL receptor double knockout mice fed a diabetogenic diet showed improved plasma cholesterol and triglyceride levels but developed obesity, hyperinsulinemia, and glucose intolerance equivalent to obese LDL receptor-deficient mice. Adipocyte hypertrophy, macrophage accumulation, and local inflammation were not attenuated in intraabdominal adipose tissue in TLR4 and LDL receptor double knockout mice. However, TLR4 deficiency led to markedly decreased atherosclerosis in obese TLR4 and LDL receptor double knockout mice. Compensatory upregulation of TLR2 expression was observed both in obese TLR4-deficient mice and in palmitate-treated TLR4-silenced 3T3-L1 adipocytes. CONCLUSIONS: TLR4 deficiency decreases atherosclerosis without affecting obesity-induced inflammation and insulin resistance in LDL receptor-deficient mice. Alternative pathways may be responsible for adipose tissue macrophage infiltration and insulin resistance that occurs in obesity.

Mechanisms underlying different responses of plasma triglyceride to high-fat diets in hamsters and mice: roles of hepatic MTP and triglyceride secretion.

Hypertriglyceridemia, closely associated with insulin resistance, is induced on high-fat diets (HFD) in humans but not in mouse models. Mechanisms underlying this species difference are still unclear. Hamsters resemble humans in lipoprotein metabolism. Here by comparing the responses to HFD in hamsters and mice, we found that hepatic TG secretion, MTP expression and plasma free fatty acid (FFA) level were increased in hamsters on HFD feeding but decreased in mice. Although hepatic steatosis and de novo lipogenesis were induced by HFD feeding in both models, cholesterol biosynthesis was inhibited in mice but not in hamsters. Moreover, in insulin deficient state, HFD increased plasma TG level, hepatic TG secretion, MTP expression and plasma FFA level in both models. In summary, distinct changes of MTP expression, in correlation with hepatic TG secretion, underlie the opposite responses of plasma TG levels to high-fat diets in hamsters and mice. Furthermore, hepatic TG secretion and MTP expression seems to be associated with plasma FFA level and cholesterol biosynthesis but not hepatic steatosis or de novo lipogenesis.

Glucose intolerance and decreased early insulin response in mice with severe hypertriglyceridemia.

Hypertriglyceridemia (HTG) is one of the key features of dyslipidemia in type 2 diabetes, caused by the overproduction and/or decreased clearance of triglyceride (TG)-rich lipoproteins, and significantly promotes the development of cardiovascular diseases in diabetes. However, the effect of severe HTG on glucose metabolism has not previously been determined. Lipoprotein lipase (LPL) deficiency results in severe HTG in humans. By using LPL-deficient mice with severe HTG, we assessed the impact of severe HTG on insulin secretion and glucose tolerance in the present study. While young LPL-deficient mice (4 months of age) showed higher fasting blood glucose (7.42 +/- 0.84 versus 4.8 +/- 0.80 mmol/L, P < 0.01) and lower insulin concentrations (0.16 +/- 0.03 versus 0.48 +/- 0.14 ng/mL, P < 0.05), old mice (12 months of age) had higher insulin (1.70 +/- 0.35 versus 0.77 +/- 0.04 ng/mL, P < 0.05) but normal fasting blood glucose concentrations. Both young and old mice had elevated free fatty acid (FFA) concentrations and exhibited decreased early insulin response; however, only old mice showed impaired glucose tolerance, as compared with wild-type mice of a similar age. Morphological assessment showed enlarged islets in old LPL-deficient mice. These findings suggest that different tests for glucose homeostasis may be needed for patients with LPL deficiency and severe HTG, even though their glucose concentrations are normal at initial screening.

[Study on the mechanism of the interaction of methylene blue and sulfation pachymaran].

In order to understand the mechanism of the interaction of sulfate polysaccharides and small molecules at molecular level, the structure of pachymaran was decorated by Wolfrom, and sulfation pachymaran (SP) was prepared. The maximum binding number (N = 54) and the binding equilibrium constant (K = 1.563 x 10(6)) of the sulfation pachymaran and methylene blue (MB) were obtained by the exoterica model. The influence of the molar ratio of MB/SP, ethanol, hydroxypropyl-beta-cyclodextrin, Triton X-100 and NaCl on the spectra of MB-SP complex was investigated. The mechanism of the color changes of methylene blue and sulfation pachymaran reaction system has been discussed. The authors draw the conclusion that the color changes result mainly from the hydrophobic interaction between methylene blue molecules binding on sulfation pachymaran on the base of the electrostatic interaction of methylene blue and sulfation pachymaran.

[Study on quantitative assay of chondroitin sulfate with a spectrophotometric method of azure A].

A simple, accurate and rapid spectrophotmeric method was proposed for the determination of chondroitin sulfate. The method was based on the absorbances of AA-CS complex at 625 nm being in proportion to the chondroitin sulfate concentrations. The linear range was 0-30 micrograms.mL-1 (R = 0.999), and the recovery range was 97.4%-103.8%. The quantities of chondroitin sulfate in different sample were determined in this way.