Market power in auction and efficiency in emission permits allocation.

This paper analyzes how to achieve the cost-effectiveness by initial allocation of CO2 emission permits when a single dominant firm in production market has market power in auction, and compare two prevalent allocation patterns, mixed allocation and single auction. We show how the firm with market power may manipulate the auction price, thereby this leads to fail to achieve cost-effective solution by auction unless the total permits for allocation equal to the effective emissions cap. Provided that the market power firm receives strictly positive free permits, the effective emissions cap of mixed allocation is larger than that of single auction. The production market share of dominant firm is increasing with the free permits it holds. Finally, we examine the compliance costs and welfare of mixed allocation and single auction, the result show that the former is preferred to the later when policy makers consider economic welfare without welfare cost due to CO2 emissions.

[Modification by wheat germ agglutinin delays the ocular elimination of liposome].

The purpose of this study is to explore the feasibility of wheat germ agglutinin (WGA) modified liposome as a vehicle for ophthalmic administration. Liposome loaded with 5-carboxyfluorescein (FAM) was prepared by lipid film hydration method. WGA was thiolated and then conjugated to the surface of the liposome via polyethylene glycol linker to constitute the WGA-modified and FAM-loaded liposome (WGA-LS/FAM). The amount of thiol groups on each WGA molecule was determined, and the bioactivity of WGA was estimated after it was modified to the surface of liposome. The physical and chemical features of the WGA-modified liposome were characterized and the ocular bioadhesive performance was evaluated in rats. The result showed that each thiolated WGA molecule was conjugated with 1.32 thiol groups. WGA-LS/FAM had a mean size of (97.40 +/- 1.39) nm, with a polydispersity index of 0.23 +/- 0.01. The entrapment efficacy of FAM was about (2.95 +/- 0.21)%, and only 4% of FAM leaked out of the liposome in 24 h. Erythrocyte agglutination test indicated that after modification WGA preserved the binding activity to glycoprotein. The in vivo ocular elimination of WGA-LS/FAM fitted first-order kinetics, and the elimination rate was significantly slower than that of the unmodified liposome, demonstrating WGA-modified liposome is bioadhesive and suitable for ophthalmic administration.

Research on the Formation Mechanism of Health Insurance Fraud in China: From the Perspective of the Tripartite Evolutionary Game.

The problem of fraud in China's health insurance has existed for a long time and is becoming more serious, which needs to be solved urgently. This article constructs a tripartite evolutionary game model to study the formation mechanism of the Health Insurance fraud, game participants including medical administrative organization (MAO, a government department responsible for health insurance supervision), medical institutions (MI, such as hospitals), and insured individuals (II, who participating in medical and healthcare insurance). By analyzing the equilibrium of the tripartite evolutionary game, this paper makes an in-depth study on the formation and resolution of health insurance fraud. The results show that: (1) How to prevent the fraud behavior of the medical institutions is the difficulty and core of the problem. It is necessary to achieve effective supervision of the MAO, improve the internal management of the MI and give play to the supervisory role of the II. (2) The regulatory behavior of the MAO needs to focus on protecting the interests of the II, not only to encourage them to actively play the role of supervision and reporting but also to prevent their collusion with MI. (3) On the one hand, the MAO needs to strengthen supervision and increase the punishment for fraud. On the other hand, they also need to take incentive measures to guide all subjects to form a sound internal management mechanism.

Potentialities and Challenges of mRNA Vaccine in Cancer Immunotherapy.

Immunotherapy has become the breakthrough strategies for treatment of cancer in recent years. The application of messenger RNA in cancer immunotherapy is gaining tremendous popularity as mRNA can function as an effective vector for the delivery of therapeutic antibodies on immune targets. The high efficacy, decreased toxicity, rapid manufacturing and safe administration of mRNA vaccines have great advantages over conventional vaccines. The unprecedent success of mRNA vaccines against infection has proved its effectiveness. However, the instability and inefficient delivery of mRNA has cast a shadow on the wide application of this approach. In the past decades, modifications on mRNA structure and delivery methods have been made to solve these questions. This review summarizes recent advancements of mRNA vaccines in cancer immunotherapy and the existing challenges for its clinical application, providing insights on the future optimization of mRNA vaccines for the successful treatment of cancer.

MK-801 changes the role of glutamic acid on modulation of algesia in nucleus accumbens.

Dizocilpine maleate (MK-801) causes the blockage of the glutamic acid (Glu) receptors in the central nervous system that are involved in pain transmission. However, the mechanism of action of MK-801 in pain-related neurons is not clear, and it is still unknown whether Glu is involved in the modulation of this processing. This study examines the effect of MK-801, Glu on the pain-evoked response of pain-excitation neurons (PENs) and pain-inhibition neurons (PINs) in the nucleus accumbens (NAc) of rats. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The electrical activities of PENs or PINs in NAc were recorded by a glass microelectrode. Our results revealed that the lateral ventricle injection of Glu increased the discharged frequency and shortened the discharged latency of PEN, and decreased the discharged frequency and prolonged the discharged inhibitory duration (ID) of PIN in NAc of rats evoked by the noxious stimulation, while intra-NAc administration of MK-801 produced the opposite response. On the basis of above findings we can deduce that Glu, MK-801 and N-methyl-D-aspartate (NMDA) receptor are involved in the modulation of nociceptive information transmission in NAc.

[Estimation of spectral reflectance using color scanner].

To obtain accurate and device-independent color, the scanner needs to be characterized. Considering that the behavior of color scanner always deviates from linear reflectance model and that the color distribution of training samples has considerable effect on the color estimation accuracy, a new spectral characterization method is proposed. This method can estimate accurate high-dimensional spectral reflectance from low-dimensional scanner responses, based on limited sample selection and weighted training. Experimental results indicate that the performance of the proposed method is obviously better than that of previous method, in both color difference error and spectral reflectance error.

Geridonin, a novel derivative of oridonin, inhibits proliferation of MGC 803 cells both in vitro and in vivo through elevating the intracellular ROS.

OBJECTIVES: To study the antitumour activity of a novel derivative of oridonin named geridonin in vitro and in vivo. METHODS: MTT and colony formation assay were used to test the cytotoxicity of geridonin; apoptosis, cell cycle arrest and the levels of reactive oxygen species were measured by flow cytometry; JC-1 staining assay was used to examine the mitochondrial membrane potential; the MGC 803 xenograft model was established to evaluate the antitumour effect of geridonin in vivo; H&E staining was performed for the histological analysis. KEY FINDINGS: In vitro, geridonin remarkably inhibited proliferation of gastrointestinal cancer cells including oesophageal, gastric, liver and colon cancers. On oesophageal, gastric cancer cells, geridonin displayed strong cytotoxicity than that of oridonin. In gastric cancer MGC 803 cells, geridonin triggered apoptosis through the mitochondrial pathway depending on caspase. In addition, geridonin sharply reduced the formation of cell colony, increased the intracellular levels of ROS and induced cell cycle arrest at G2/M phase. In vivo, geridonin delayed the growth of MGC 803 xenograft in athymic mice without obvious loss of bodyweight. CONCLUSIONS: The novel derivative of oridonin, geridonin, inhibited the growth of human gastric cancer cells MGC 803 both in vitro and in vivo mainly via triggering apoptosis depending on elevating intracellular level of ROS.

Design and synthesis of isatin/triazole conjugates that induce apoptosis and inhibit migration of MGC-803 cells.

A series of new isatin/triazole conjugates were designed based on the hypothesis that the ester-linked compounds could be enzymatically hydrolyzed by cellular esterases inside the cells. These compounds showed moderate to good growth inhibition toward the tested cancer cells, exerted selective inhibition toward MGC-803 cells and were less toxic to normal cells HL-7702 and GES-1. Of these compounds, compound 5a showed the best inhibitory activity against MGC-803 cells (IC50 = 9.78 µM), induced apoptosis through multiple mechanisms, as well as inhibited migration of MGC-803 cells.

Geridonin and paclitaxel act synergistically to inhibit the proliferation of gastric cancer cells through ROS-mediated regulation of the PTEN/PI3K/Akt pathway.

Paclitaxel, a taxane, is a cytotoxic chemotherapeutic agent that targets microtubules. It has become a front-line therapy for a broad range of malignancies, including lung, breast, gastric, esophageal, and bladder carcinomas. Although paclitaxel can inhibit tumor development and improve survival, poor solubility, myelotoxicity, allergic reactions, and drug resistance have restricted its clinical application. Paclitaxel is frequently combined with other chemotherapeutics to enhance the antitumor effects and reduce side effects. We synthesized geridonin, a derivative of oridonin, and demonstrate that geridonin and paclitaxel act synergistically to inhibit the growth of gastric cancer cells. Importantly, geridonin enhanced the antitumor effects of paclitaxel without increasing toxicity in vivo. Mechanistic analysis revealed that administration of geridonin in combination with paclitaxel up-regulated the tumor suppressor PTEN and inhibited phosphorylation of Akt and MDM2. This led to the accumulation of p53 and induced apoptosis though the mitochondrial pathway. Thus, geridonin in combination with paclitaxel is a new treatment strategy for gastric cancer.

Design, synthesis and biological evaluation of [1,2,3]triazolo[4,5-d]pyrimidine derivatives possessing a hydrazone moiety as antiproliferative agents.

A series of [1,2,3]triazolo[4,5-d]pyrimidine derivatives bearing a hydrazone moiety were designed, synthesized and evaluated for their antiproliferative activity against several cancer cell lines of different origins by MTT assay. Most of the synthesized compounds demonstrated moderate to good activity against the cancer cell lines selected. Especially, compound 43 showed the most potent antiproliferative activity as well as good selectivity between cancer and normal cells (IC50 values of 0.85 µM against MGC-803 and 56.17 µM against GES-1). In addition, compound 43 evidently inhibited the colony formation of MGC-803 cells at 0.8 µM. Further mechanism studies revealed that compound 43 could induce apoptosis of MGC-803 cells probably through the mitochondrial pathway accompanied with decrease of the mitochondrial membrane potential (MMP), activations of caspase-9/3, up-regulation of the expression of Bax, Bak and PUMA, as well as down-regulation of that of Bcl-2 and Mcl-1.

Effects of norepinephrine on the electrical activities of pain-related neurons in the rat nucleus accumbens.

This study examined the effects of norepinephrine (NE) and phentolamine on the electrical activities of pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the nucleus accumbens (NAc) of Wistar rats. Trains of electric pulses applied to the right sciatic nerve were used to provide noxious stimulation, and the discharges of PENs and PINs were recorded using a glass microelectrode. Our results revealed that in response to noxious stimulation, NE decreases the evoked discharge frequency of PENs and increases the evoked discharge frequency of PINs in the NAc of healthy rats, whereas phentolamine produced opposite responses. These results demonstrate that NE is involved in the modulation of nociceptive information transmission in the NAc.

L-365,260 reversed effect of sincalide against morphine on electrical and mechanical activities of rat duodenum in vitro.

AIM: To study the antagonism of sincalide (CCK-8) to the effect of morphine and its mechanism. METHODS: The electrical and mechanical activities of rat duodenum in vitro were recorded simultaneously. RESULTS: Acetylcholine (ACh, 300 nmol/L) increased the spike potential amplitude (SPA) and the number (SPN) of rat duodenum in vitro, followed by an increase of duodenal contraction amplitudes (CA). The SPA, SPN, and CA of duodenum in vitro were not obviously affected by injection of morphine (330 nmol/L), but it could selectively inhibit the potentiation of ACh. After administration of CCK-8 (0.7 nmol/L), the SPA, SPN, and CA of duodenal segment did not exhibit obvious changes. But CCK-8 could selectively antagonize the effects of morphine, ie, the SPA and SPN were increased again, followed by an increase of CA. CCK-B receptor antagonist L-365,260 (30 nmol/L) reversed the antagonism of CCK-8 to the effect of morphine. CONCLUSION: CCK-8 could selectively antagonize the effect of morphine which inhibited the potentiation of ACh on duodenal activities in vitro. The antagonistic effect of CCK-8 on morphine was mainly mediated by CCK-B receptor.

Effect of devazepide reversed antagonism of CCK-8 against morphine on electrical and mechanical activities of rat duodenum in vitro.

AIM:To study the antagonism of cholecystokinin octapeptide (CCK-8) against the effect of morphine and its mechanism.METHODS:The method of simultaneously recording the electrical and mechanical activities of rat duodenum in vitro was adopted.RESULTS:Acetylcholine (ACh) could increase the amplitude and the number of the spike potential (SPA and SPN of rat duodenum in vitro, followed by the increase of the duodenal contraction amplitudes (CA), showing a positive correlation. Morphine, on the contrary, inhibited the potentiation of ACh, showing a negative correlation. CCK-8 could antagonize the effects of morphine, i.e. th SPA and SPN were increased again, followed by the increase of CA. On the basis of the above, CCK-A receptor antagonist Devazepide could reverse the antagonism of CCK-8 to the effect of morphine.CONCLUSION:CCK-8 could antagonize the effect of morphine which inhibited the potentiation of ACh on the duodenal activities in vitro.Furthermore, it was inferred that the antagonistic effect of CCK-8 on morphine was mainly mediated by CCK-A receptor.