Fulvic acid alleviates cadmium-induced root growth inhibition by regulating antioxidant enzyme activity and carbon-nitrogen metabolism in apple seedlings.

Introduction: Substantial previous studies have reported that fulvic acid (FA) application plays an important role in Chinese agricultural production. However, little is known about the mechanisms for using FA to increase apple trees resistance to Cd toxicity. In order to clarify the mechanism underlying FA alleviation in Cd-induced growth inhibition in apple seedlings. Methods: Herein, we treated M9T337 seedlings to either 0 or 30 µM/L Cd together with 0 or 0.2 g/L FA and analyzed the root growth, antioxidant enzyme activities, carbon (C) assimilation, nitrogen (N) metabolism, and C and N transport. Results: The results presented that, compared with CK (without Cd addition or FA spraying application), Cd poisoning significantly inhibited the root growth of apple seedlings. However, this Cd-induced root growth inhibition was significantly alleviated by FA spraying relative to the Cd treatment (Cd addition alone). On the one hand, the mitigation of inhibition effects was due to the reduced oxidative damage by enhancing antioxdiant enzyme (SOD, POD, and CAT) activities in leaves and roots. On the other hand, this growth advantage demonstrated compared to the Cd treatment was found to be associated with the strengthen of photosynthetic performance and the elevation of C and N metabolism enzymes activities. Meanwhile, we also found that under Cd stress condition, the distribution of C and N nutrients in apple seedlings was optimised by FA spraying application relative to the Cd treatment, according to the results of 13C and 15N tracing. Conclusion: Conclusively, our results suggested that the inhibitory effect of Cd on apple seedlings root growth was alleviated by FA through regulating antioxdiant capacities and C and N metabolism.

PI3Kα inhibitor GNE-493 triggers antitumor immunity in murine lung cancer by inducing immunogenic cell death and activating T cells.

Phosphatidylinositol 3-kinase (PI3K) is frequently hyperactivated in cancer, playing pivotal roles in the pathophysiology of both malignant and immune cells. The impact of PI3K inhibitors on the tumor microenvironment (TME) within lung cancer remains largely unknown. In this study, we explored the regulatory effects of GNE-493, an innovative dual inhibitor of PI3K and mammalian target of rapamycin (mTOR), on the TME of lung cancer. First, through the analysis of The Cancer Genome Atlas-lung squamous cell carcinoma (LUSC) cohort, we found PIK3CA to be related to CD8 T cells, which may affect the overall survival rate of patients by affecting CD8 function. We herein demonstrated that GNE-493 can significantly inhibit tumor cell proliferation and promote cell apoptosis while increasing the expression of the immunogenic death-related molecules CRT and HSP70 using in vitro cell proliferation and apoptosis experiments on the murine KP lung cancer cell line and human A549 lung cancer cell line. Next, through the establishment of an orthotopic tumor model in vivo, it was found that after GNE-493 intervention, the infiltration of CD4+ and CD8+ T cells in mouse lung tumor was significantly increased, and the expression of CRT in tumors could be induced to increase. To explore the mechanisms underlying PI3K inhibition-induced changes in the TME, the gene expression differences of T cells in the control group versus GNE-493-treated KP tumors were analyzed by RNA-seq, and the main effector pathway of anti-tumor immunity was identified. The IFN/TNF family molecules were significantly upregulated after GNE-493 treatment. In summary, our findings indicate that GNE-493 promotes immunogenic cell death in lung cancer cells, and elucidates its regulatory impact on molecules associated with the adaptive immune response. Our study provides novel insights into how PI3K/mTOR inhibitors exert their activity by modulating the tumor-immune interaction.

Granule Dendrobii suppresses chronic atrophic gastritis induced by N-methyl-N'-nitro-N-nitrosoguanidine by modulating the gastrointestinal bacteria in rats.

Chronic atrophic gastritis (CAG) is an important stage in the transformation of the normal gastric mucosa into gastric cancer. Granule Dendrobii (GD), a proprietary Chinese medicine, has proven clinical efficacy in treating CAG. GD might promote the reversal of precancerous lesions by improving them in CAG patients. However, the mechanism of GD in CAG treatment is relatively less understood. Here, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced CAG rats were treated with GD and its efficacy was evaluated by observing the changes in the rats' weight and the pathology of gastric tissues. The potential effect of GD on the bacteria was predicted and verified in the large and small intestines and stomachs of CAG rats using amplicon sequencing and RT-qPCR. The results showed that GD could ameliorate the symptoms of body weight loss in CAG rats. Hematoxylin-Eosin (HE) and Alcian Blue (AB) staining showed that GD significantly improved the pathological state of the gastric mucosa in CAG rats. The relative abundance (RA) of Lactobacillus and Turicibacter significantly decreased after GD intervention compared with that of the model group (P < 0.05), indicating that GD might improve CAG by regulating the RA of Lactobacillus and Turicibacter. These findings revealed that Lactobacillus and Turicibacter as bacteria agents associated with gastritis, have the potential to inhibit gastric cancer, especially Turicibacter maybe another pathogen of CAG besides Helicobacter pylori (HP), which is worthy of further study. Meanwhile, the findings provided new ideas and materials for the research and development of new CAG drugs.

Transcriptome and metabolome analysis of flavonol synthesis in apricot fruits.

Introduction: Apricot fruits are edible and serve as a source of medicinal compounds. Flavonols are important plant secondary metabolites that have antioxidant and antitumor effects and may promote cardiovascular health. Methods: The flavonoid content in three stages of the 'Kuijin' and the 'Katy' was observed, followed by the combination of metabolome and transcriptome analysis to explore the metabolic basis of flavonol synthesis. Results: The differences in the metabolite contents between stages (of the same cultivar) and between cultivars (at the same stage) revealed decreases in the flavonoid content as fruits developed (i.e., from 0.28 mg/g to 0.12 mg/g in 'Kuijin' and from 0.23 mg/g to 0.05 mg/g in 'Katy'). To decipher the regulation of flavonol synthesis in apricot (Prunus armeniaca L.), the metabolomes and transcriptomes of fruit pulp at three developmental stages of 'Kuijin' and the 'Katy' were analyzed. A total of 572 metabolites were detected in 'Kuijin' and the 'Katy' pulp, including 111 flavonoids. The higher flavonol content young 'Kuijin' fruits at 42 days after full bloom is mainly due to 10 types of flavonols. Three pairs of significant differences in flavonol content were identified. From these three comparison groups, three structural genes were strongly correlated with the levels of 10 types of flavonols (Pearson correlation coefficients > 0.8, p value < 0.05), including PARG09190, PARG15135, and PARG17939. The weighted gene co-expression network analysis showed that the turquoise module genes were highly correlated with flavonol contents (P < 0.01). There were 4897 genes in this module. Out of 4897 genes, 28 transcription factors are associated with 3 structural genes based on weight value. Two of the transcription factors are not only associated with PARG09190 but also with PARG15135, indicating their critical importance in the flavonols biosynthesis. The two TFs are PARG27864 and PARG10875. Discussion: These findings provide new insights into the biosynthesis of flavonols and may explain the significant differences in flavonoid content between the 'Kuijin' and the 'Katy' cultivars. Moreover, it will aid in genetic improvement to enhance the nutritional and health value of apricots.

Yiwei decoction promotes apoptosis of gastric cancer cells through spleen-derived exosomes.

Yiwei decoction (YWD) is a formula of traditional Chinese medicine (TCM) that is clinically effective for the prevention and treatment of gastric cancer recurrence and metastasis. According to the theory of TCM, YWD tonifies the body and strengthens the body's resistance to gastric cancer recurrence and metastasis potentially via the immune regulation of the spleen. The aims of the present study were to investigate whether YWD-treated spleen-derived exosomes in rats inhibit the proliferation of tumor cells, to elucidate the anticancer effects of YWD, and to provide evidence supporting the use of YWD as a new clinical treatment for gastric cancer. Spleen-derived exosomes were obtained by ultracentrifugation and identified by transmission electron microscopy, nanoparticle tracking analysis, and western blot analysis. The location of the exosomes in tumor cells was then determined by immunofluorescence staining. After tumor cells were treated with different concentrations of exosomes, the effect of exosomes on cell proliferation was determined by cell counting kit 8 (CCK8) and colony formation assays. Tumor cell apoptosis was detected by flow cytometry. Particle analysis and western blot analysis identified the material extracted from spleen tissue supernatant as exosomes. Immunofluorescence staining showed that spleen-derived exosomes were taken up by HGC-27 cells, and the CCK8 assay confirmed that the relative tumor inhibition rate of YWD-treated spleen-derived exosomes in the 30 µg/mL reached 70.78% compared to control exosomes in the 30 µg/mL (p < 0.05). Compared to control exosomes in the 30 µg/mL, the colony formation assay indicated that YWD-treated spleen-derived exosomes in the 30 µg/mL colonies have decreased by 99.03% (p < 0.01). Moreover, flow cytometry analysis showed that treatment with YWD-treated exosomes in the 30 µg/mL increased the apoptosis rate to 43.27%, which was significantly higher than that of the control group in the 30 µg/mL (25.91%) (p < 0.05). In conclusion, spleen-derived exosomes from YWD-treated animals inhibit the proliferation of HGC-27 cells via inducing apoptosis, suggesting that spleen-derived exosomes are involved in mediating the antitumor effect of YWD. These results demonstrated a novel exosome-mediated anticancer effect of YWD as a TCM formula, thereby supporting the use of YWD-treated exosomes as a new approach for the clinical treatment of gastric cancer.

Experimental evidence of shikonin as a novel intervention for anti-inflammatory effects.

Shikonin is a natural product with antioxidant and anti-inflammatory activities. The biological activity of shikonin is still not fully understood, as well as its association with innate immunity and immune and inflammatory bowel disease (IBD) in humans. In this study, the toxicity of shikonin on Raw264.7 cells was assayed by MTT, and polarization of inflammatory macrophages was determined by flow cytometry. The results showed that shikonin can inhibit the polarization of macrophages towards M1 type and significantly inhibited the production of NO in the concentration range of 0.5-1 µM. In addition, after treatment with shikonin, the production of IL-1ß and TNF-α was significantly decreased. After shikonin administration, the body weight loss and decrease of colon length were significantly suppressed in DSS-treated colitis C57BL/6 mice. The pro-inflammatory cytokines TNF-α and IL-1ß in colonic homogenate were significantly decreased. Shikonin treatment resulted in a notable improvement in the histopathological manifestations in DSS-treated animals at 25/50 mg/kg. Meanwhile, we found that shikonin can regulate differentiation of T helper 17 cell (Th17)/regulatory T cell (Treg), thereby regulating the balance of Th17/Treg cells and exerting an anti-inflammatory effect in IBD animal models. In conclusion, we found that shikonin protects against DSS-induced acute colitis by, among other things, reducing immune cell infiltration, polarizing macrophages, and regulating Th17/Treg differentiation, as well as by downregulating the release of inflammatory cytokines. These findings showed that shikonin can improve inflammation by affecting macrophage polarization. Our experimental data provide experimental evidence and theory basis for research on anti-inflammatory effects for the shikonin as health or functional food.

Residual levels and dietary intake risk assessment of 11 pesticides in apricots from different ecological planting regions in China.

The frequent and massive use of pesticides has led to pesticide residues in apricot, threatening food safety and human health. A reliable and simple modified QuEChERS method with ultra-performance liquid chromatography-tandem mass spectrometry was developed for the simultaneous determination of 11 pesticides in apricot. Method validation indicated that satisfied linearity (R2 ≥ 0.9959), accuracy (recoveries of 72-119%), sensitivity (limits of detection, 0.03-0.30 µg/kg; limits of quantification, 0.13-1.00 µg/kg), and precision (relative standard deviations ≤ 11.9%), and matrix effects were 0.89-1.13. Apricot samples from different ecological regions in China were collected and tested using the proposed methods. Monitoring results were used to assess the dietary intake risk of Chinese populations of different ages and genders. Dietary risk assessment revealed that the risk quotients were 0.003-1.184% for different gender and age groups in China, indicating none unacceptable public health risk for general population. This work was thus significant in developing a simpler, more efficient and economical analysis method and food safety risks of the 11 pesticides on apricot and facilitated the establishment of maximum residue limits.

Effects of Granule Dendrobii on chronic atrophic gastritis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats.

BACKGROUND: Dendrobium officinale is an herb of Traditional Chinese Medicine (TCM) commonly used for treating stomach diseases. One formula of Granule Dendrobii (GD) consists of Dendrobium officinale and American Ginseng (Radix Panacis quinquefolii), and is a potent TCM product in China. Whether treatment with GD can promote gastric acid secretion and alleviate gastric gland atrophy in chronic atrophic gastritis (CAG) requires verification. AIM: To determine the effect of GD treatment on CAG and its potential cellular mechanism. METHODS: A CAG model was induced by feeding rats N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for 12 wk. After oral administration of low, moderate, and high doses of GD in CAG rats for 8 wk, its effects on body weight, gastric mucosa histology, mucosal atrophy, intestinal metaplasia, immunohistochemical staining of proliferating cell nuclear antigen (PCNA) and B-cell lymphoma-2, and hemoglobin and red blood cells were examined. RESULTS: The body weights of MNNG-induced CAG model rats before treatment (143.5 ± 14.26 g) were significantly lower than that of healthy rats (220.2 ± 31.20 g, P < 0.01). At the 8th week of treatment, the body weights of rats in the low-, moderate-, and high-dose groups of GD (220.1 ± 36.62 g) were significantly higher than those in the untreated group (173.3 ± 28.09 g, all P < 0.01). The level of inflammation in gastric tissue of the high-dose group (1.68 ± 0.54) was significantly reduced (P < 0.01) compared with that of the untreated group (3.00 ± 0.00, P < 0.05). The number and thickness of gastric glands in the high-dose group (31.50 ± 6.07/mm, 306.4 ± 49.32 µm) were significantly higher than those in the untreated group (26.86 ± 6.41/mm, 244.3 ± 51.82 µm, respectively, P < 0.01 and P < 0.05), indicating improved atrophy of gastric mucosa. The areas of intestinal metaplasia were significantly lower in the high-dose group (1.74% ± 1.13%), medium-dose group (1.81% ± 0.66%) and low-dose group (2.36% ± 1.08%) than in the untreated group (3.91% ± 0.96%, all P < 0.01). The expression of PCNA in high-dose group was significantly reduced compared with that in untreated group (P < 0.01). Hemoglobin level in the high-dose group (145.3 ± 5.90 g/L), medium-dose group (139.3 ± 5.71 g/L) and low-dose group (137.5 ± 7.56 g/L) was markedly increased compared with the untreated group (132.1 ± 7.76 g/L; P < 0.01 or P < 0.05). CONCLUSION: Treatment with GD for 8 wk demonstrate that GD is effective in the treatment of CAG in the MNNG model by improving the histopathology of gastric mucosa, reversing gastric atrophy and intestinal metaplasia, and alleviating gastric inflammation.

Proteomic analysis suggests that monoterpenes in lemongrass disrupt Ca2+ homeostasis in Haemaphysalis longicornis leading to mitochondrial depolarization and cytotoxicity.

Complex mixtures of bioactive ingredients in plant essential oils present complex chemistries which involve different modes of action. An increasing body of scientific reports has recently focused on the acaricidal activities of plant essential oils attributed to their monoterpene components, but information about their underlying molecular mechanism of action is scarce. Here, after the chemical analysis of lemongrass oil, a proteomic analysis of the ovary, salivary gland, and midgut of Haemaphysalis longicornis exposed to Cymbopogon citratus (lemongrass) essential oil was performed via data-independent acquisition mass spectrometry (DIA-MS) technology to further elucidate the molecular mechanisms involved. Pathway analysis reveals the activation of metabolic pathways mediated by oxidoreductases and transferases. Furthermore, the upregulation of various calcium-associated proteins and the upregulation of cytochrome c1, cytochrome c oxidase polypeptide IV, and programmed cell death protein 6-like isoform X1 suggest a cytotoxic mode of action via the formation of reactive oxygen species (ROS), mitochondrial Ca2+ overload, mitochondrial uncoupling, and depolarization, and ATP depletion leading to either apoptotic or necrotic death. Morphological alterations observed after the RNAi of a major detoxification enzyme (glutathione S-transferase) merit further investigation. Hence, the cytotoxic mode of action exhibited by C. citratus oil could be vital for the development of eco-friendly acaricide.

Comprehensive dynamic analysis of proteins in the spermatheca of female Haemaphysalis longicornis after copulation.

Ticks are obligate blood-sucking parasitic arthropods. When sucking the blood of hosts, they can also transmit a variety of pathogens to hosts that severely endanger the health of humans and animals. The spermatheca is an organ for the storage and protection of sperm and an important component of the reproductive system of female ticks. The spermatheca content changes dramatically over time after copulation. In particular, some proteins and polypeptide substances can influence the physiological functions of female ticks and promote blood feeding and egg laying by female ticks. To investigate the molecular mechanisms underlying the productive process of Haemaphysalis longicornis, data-independent acquisition (DIA) quantitative proteomics technology was used to perform in-depth research of the dynamic changes in all proteins in the spermatheca of ticks within a short time after copulation to look for key proteins in the spermatheca contents after copulation that affect the reproduction of female ticks in order to provide meaningful information for the comprehensive prevention and control of ticks.

Effects of metamitron on fruit set and photosynthetic biological characteristics of apples.

With dwarfing interstock Fuji apples as the test materials and water treatment as the control (CK), we examined the fruit thinning effect and its influences on leaves' photosynthesis by spraying 200, 300, and 400 mg·L-1 metamitron during the young fruit period to solve artificial fruit thinning problems (time-consuming, much labor, and low efficiency). The results showed that metamitron application could significantly reduce the inflorescence and flowers' fruit-setting rate by 16.5%-22.8% and 50.9%-53.9%, respectively. The treatment of 300 mg·L-1 metamitron had the strongest fruit thinning effect, with a single fruit rate of 46.6% and a double fruit rate of 18.3%. As a photosynthesis inhibitor, metamitron application reduced the chlorophyll content of leaves and strongly affected photosynthesis. The inhibitory effect on chlorophyll content disappeared after 15 days of the treatment, while that on the net photosynthetic rate disappeared gradually after 11 days of the treatment. The application of metamitron significantly reduced the maximum quantum yield of PSⅡ reaction center (Fv/Fm), actual photochemical efficiency (ΦPSⅡ), photochemical quenching coefficient (qP) and non-photochemical quenching coefficient (NPQ), with such inhibitory effect having been lasted for 15 days. OJIP analysis showed that metamitron caused damage to the apple leaves' oxygen-evolving complex, especially limiting the transfer of electrons in the PSⅡ reaction center from QA to QB. Metamitron treatment increased Wk, and significantly decreased ψo, RC/CSm, and PIabs. Besides, 300 mg·L-1 metamitron had the most significant effect. Our results showed that metamitron destroyed the structure of the PSⅡ reaction center of apple leaves and hindered the transfer of electrons from the donor to the receptor of PSⅡ. Consequently, the photosynthetic rate was affected, and the young fruits fell off due to the lack of accumulation of photosynthetic products.

Protein regulation strategies of the mouse spleen in response to Babesia microti infection.

BACKGROUND: Babesia is a protozoan parasite that infects red blood cells in some vertebrates. Some species of Babesia can induce zoonoses and cause considerable harm. As the largest immune organ in mammals, the spleen plays an important role in defending against Babesia infection. When infected with Babesia, the spleen is seriously injured but still actively initiates immunomodulatory responses. METHODS: To explore the molecular mechanisms underlying the immune regulation and self-repair of the spleen in response to infection, this study used data-independent acquisition (DIA) quantitative proteomics to analyse changes in expression levels of global proteins and in phosphorylation modification in spleen tissue after Babesia microti infection in mice. RESULTS: After mice were infected with B. microti, their spleens were seriously damaged. Using bioinformatics methods to analyse dynamic changes in a large number of proteins, we found that the spleen still initiated immune responses to combat the infection, with immune-related proteins playing an important role, including cathepsin D (CTSD), interferon-induced protein 44 (IFI44), interleukin-2 enhancer-binding factor 2 (ILF2), interleukin enhancer-binding factor 3 (ILF3) and signal transducer and activator of transcription 5A (STAT5A). In addition, some proteins related to iron metabolism were also involved in the repair of the spleen after B. microti infection, including serotransferrin, lactoferrin, transferrin receptor protein 1 (TfR1) and glutamate-cysteine ligase (GCL). At the same time, the expression and phosphorylation of proteins related to the growth and development of the spleen also changed, including protein kinase C-δ (PKC-δ), mitogen-activated protein kinase (MAPK) 3/1, growth factor receptor-bound protein 2 (Grb2) and P21-activated kinase 2 (PAK2). CONCLUSIONS: Immune-related proteins, iron metabolism-related proteins and growth and development-related proteins play an important role in the regulation of spleen injury and maintenance of homeostasis. This study provides an important basis for the diagnosis and treatment of babesiosis.

Possible Novel Therapeutic Targets in Lymphangioleiomyomatosis Treatment.

Lymphangioleiomyomatosis (LAM) is a rare systemic neoplastic disease that exclusively happens in women. Studies focusing on LAM and tuberous sclerosis complex (TSC) have made great progress in understanding the pathogenesis and searching for treatment. The inactive mutation of TSC1 or TSC2 is found in patients with LAM to activate the crucial mammalian target of rapamycin (mTOR) signaling pathway and result in enhanced cell proliferation and migration. However, it does not explain every step of tumorigenesis in LAM. Because cessation of rapamycin would break the stabilization of lung function or improved quality of life and lead to disease recurrent, continued studies on the pathogenesis of LAM are necessary to identify novel targets and new treatment. Researchers have found several aberrant regulations that affect the mTOR pathway such as its upstream or downstream molecules and compensatory pathways in LAM. Some therapeutic targets have been under study in clinical trials. New methods like genome-wide association studies have located a novel gene related to LAM. Herein, we review the current knowledge regarding pathogenesis and treatment of LAM and summarize novel targets of therapeutic potential recently.

Phosphoproteomic Analysis of X enopus laevis Reveals Expression and Phosphorylation of Hypoxia-Inducible PFKFB3 during Dehydration.

Xenopus laevis tolerate dehydration when their environments evaporate during summer months. Protein phosphorylation has previously shown to regulate important adaptations in X. laevis, including the transition to anaerobic metabolism. We therefore performed phosphoproteomic analysis of X. laevis to further elucidate the cellular and metabolic responses to dehydration. Phosphoproteins were enriched in cellular functions and pathways related to glycolysis/gluconeogenesis, the TCA cycle, and protein metabolism, among others. The prominence of phosphoproteins related to glucose metabolism led us to discover that the hypoxia-inducible PFKFB3 enzyme was highly phosphorylated and likely activated during dehydration, a feature of many cancers. Expression of the four transcript variants of the pfkfb3 gene was found all to be upregulated during dehydration, potentially due to the enrichment of hypoxia responsive elements in the pfkfb3 promoter. These results further support the role of anaerobic glycolysis during dehydration in X. laevis and elucidate a potential mechanism for its increased rate.

The association between small tumor size and poor survival in T4 mucinous adenocarcinoma of colon without distant metastasis.

PURPOSE: The purpose of this study was to analyze the impact of tumor size on cancer-specific survival (CSS) in patients with mucinous adenocarcinoma (MAC) of the colon, showing heavy intestinal wall invasion without distant metastasis (T4 N0-2 M0). METHODS: Patients with T4N0-2M0 MAC of colon were analyzed based on data from the US Surveillance, Epidemiology, and End Results (SEER) database. Survival was analyzed using the Kaplan-Meier method, and the log-rank test was used to identify differences. Risk factors were analyzed using the Cox proportional hazard model. A preliminary analysis of T4N0-2M0 adenocarcinoma of colon patients from the SEER database is also presented. RESULTS: A total of 585 patients from the SEER database were included in the analysis. The cutoff value (5.0 cm) was determined using the X-tile program. Kaplan-Meier analysis showed that tumors ≤5.0 cm had a poorer CSS compared to tumors >5.0 cm (p=0.034). Multivariate analysis indicated that tumor size is an independent prognostic factor for these patients, and compared to tumors ≤5.0 cm, tumors >5.0 cm were more likely to have better CSS (HR 0.658, 95% CI 0.506-0.854, p=0.002). Tumor size was also analyzed as a continuous variable in multivariate analysis, and CSS decreased with decreasing tumor size (HR 0.919, 95% CI 0.873-0.968, p<0.001). No significant association between tumor size and CSS was observed in patients with T4N0- 2M0 MAC of the colon. CONCLUSION: Smaller tumor size is associated with poorer CSS in patients with T4N0-2M0 MAC of the colon.

A novel GAP460 biopolymer for use as a carrier in drug-delivery applications.

We synthesized a new non-toxic biopolymer (GAP460) containing γ,L-glutamic acid and aspartate (Asp). Conjugates of GAP460 and cisplatin exhibited a drug-carrying capacity of nearly 40%, 3-times higher than γ-PGA and dramatically decreasing the amount of biopolymer required for high-dose delivery. Treatment with GAP460-cisplatin conjugate (PACC) not only effectively inhibited tumor growth in nude mice, but also resulted in extended survival and lower nephrotoxicity, suggesting that GAP460 could be used as an effective carrier for drug delivery and that PACC may have potential therapeutic applications in the clinical treatment of cancer.

Decomposition of 1,2-dichloroethane over CeO2 modified USY zeolite catalysts: effect of acidity and redox property on the catalytic behavior.

CeO(2) modified ultrastable Y zeolite (CeO(2)-USY) catalysts were prepared and were used as the catalysts for the decomposition of 1,2-dichloroethane (DCE). The catalytic behavior of these catalysts was evaluated by micro-reaction and temperature-programmed surface reaction (TPSR) technique. The results reveal that CeO(2)-USY catalysts exhibit good catalytic activity for DCE decomposition and high selectivity to the formation of CO(2) and HCl. Both acidity and redox property play important roles in the DCE decomposition, and the synergy between CeO(2) species and USY zeolite shows an enhancement in the catalytic activity for DCE decomposition. CeO(2)-USY (1:8) with high dispersion of CeO(2) species and a much more suitable combination of acidity and redox property exhibits the best catalytic activity.