Anthracycline chemicals with anthracyclinone structure exert antitumor effects by inhibiting angiogenesis and lymphangiogenesis in a xenografted gastric tumor model.

BACKGROUND: It is vital to screen or develop alternative therapeutic drugs with higher curative characteristics and fewer side effects for the clinical treatment of gastric cancer. METHODS: Gastric cancer cells were exposed to different auramycin G doses while determining the impact on cell viability, migration, and invasion. Then the antitumor effects of auramycin G, 5-fluorouracil (5-Fu) and their combination were evaluated. Furthermore, the molecular mechanisms of angiogenesis and lymphangiogenesis regulated by auramycin G and its analogs were investigated. RESULTS: Auramycin G inhibited cell viability in a dose-dependent manner, with a 50% inhibitory concentration of 23.72 ± 6.36 mg/L and 32.54 ± 5.91 mg/L for AGS and MGC803 cells, respectively. The migration and invasion of gastric cancer cells were significantly inhibited by 10 mg/L auramycin G, which was consistent with the down-regulation of the VEGFR2-VEGFA-pPI3K-pAkt-pErk1 and VEGFR3-VEGFC-pPI3K-pAkt-pmTOR proteins. Notably, the average tumor weights were significantly reduced in both the auramycin G (2.21 ± 0.45 g) of 50 mg/kg body weight and auramycin G + 5-fluorouracil (5-Fu) groups (1.33 ± 0.28 g), compared with the control (3.73 ± 0.56 g). Considering that auramycin G decreased the growth of blood and lymphatic vessels while reducing the degree of tumor malignancy, it effectively suppressed tumors by regulating the angiogenic and lymphangiogenic pathways. CONCLUSION: The present study confirmed that auramycin G displayed a prominent antitumor activity in gastric tumor models, both in vitro and in vivo. Moreover, it was confirmed that auramycin G played a specific role in certain gastric cancer cell types, while the mechanism was validated to be associated with angiogenesis- and lymphangiogenesis-related pathway suppression.

Rational design of hierarchically nanostructured NiTe@CoxSy composites for hybrid supercapacitors with impressive rate capability and robust cycling durableness.

The hierarchically nanostructured NiTe@CoxSy composites are constructed on a foamed nickel substrate by a two-step electrode preparation process. Structural characterization shows the dense growing of CoxSy nanosheets around NiTe nanorods forms a hierarchical nanostructure which possesses synergetic effects from both compositional and structural complementarity, more pathways for ion/electrolyte transport, richer redox active sites, and better conductivity. Thanks to the rational design of this hierarchical structure, NiTe@CoxSy delivers a high areal capacitance of 7.7F cm-2 at 3 mA cm-2 and achieves the improved capacitance retention of 97.9% after 10,000 cycles. Of particular importance is the successful fabrication of NiTe@CoxSy//activated carbon hybrid supercapacitors. This hybrid device has a wide operating voltage window, high areal energy density of 0.48 mWh cm-2 at 2.55 mW cm-2, impressive rate capability of 62.3% even after a 20-fold increase of the current density, and a 115.1% of initial capacitance retention after 15,000 cycles. Meanwhile, two tandem such hybrid devices can easily drive a pair of mini fans or light up a heart-like pattern assembled by 10 red LEDs. These experimental results not only demonstrate that the hierarchically nanostructured NiTe@CoxSy composites can serve as a prospective candidate electrode; but also develop a novel strategy about how to achieve high-performance stockpile equipment by rationale designing a desirable nanostructures.

CQMUH-011 Inhibits LPS-Induced Microglia Activation and Ameliorates Brain Ischemic Injury in Mice.

Excessive microglial activation-mediated neuroinflammation is closely involved in the pathogenesis of several neurological diseases. CQMUH-011, as a novel adamantane sulfonamide compound, has been shown anti-inflammatory properties in activated macrophages (RAW264.7). However, the role of CQMUH-011 in microglial activation-induced neuroinflammation and neuroprotective properties has yet to be elucidated. In the present study, we investigated the potential effects and mechanisms of CQMUH-011 on lipopolysaccharide (LPS)-stimulated primary microglia in vitro and transient middle cerebral artery occlusion (t-MCAO)-induced acute cerebral ischemia/reperfusion (I/R) injury in vivo. The results demonstrated that CQMUH-011 significantly suppressed the production of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß by LPS-stimulated primary microglia. In addition, CQMUH-011 inhibited the proliferation of activated microglia by arresting the cell cycle at the G1/S phase accompanied by downregulating the expression of cell cycle regulatory proteins such as proliferating cell nuclear antigen (PCNA) and cyclin D1. CQMUH-011 was seen to induce apoptosis in activated microglia by regulating the expression of Bax and Bcl-2. Furthermore, CQMUH-011 markedly attenuated the protein expression of Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) as well as the phosphorylation levels of nuclear factor-kappa (NF-κB) subunit p65, inhibitory kappa B-alpha (IκBα), and mitogen-activated protein kinases (MAPKs) such as extracellular signal-regulated kinase (ERK) and p38 kinases. In vivo, CQMUH-011 administration significantly improved neurological function and infarct volume, and ameliorated the inflammatory cytokines and microglia amount around the injury site of mice. In conclusion, these results suggested that CQMUH-011 has a notable anti-inflammatory effect and protects mice from I/R injure. Thus, CQMUH-011 may be a candidate drug for the treatment of cerebral ischemia patients.

Bone marrow mesenchymal stem cells inhibit cardiac hypertrophy by enhancing FoxO1 transcription.

Bone marrow-derived mesenchymal stem cells (BMSCs) have therapeutic potential for certain heart diseases. Previous studies have shown that stem cells inhibit cardiac hypertrophy; however, it is necessary to explore the mechanisms underlying this effect. This study aimed to investigate the possible mechanism underlying the inhibitory effect of BMSCs on cardiomyocyte hypertrophy. We induced cardiomyocyte hypertrophy in cultured rat cells through isoproterenol (ISO) treatment with or without BMSC coculture. A microarray was performed to analyze messenger RNA expression in response to ISO treatment and BMSC coculture. Pathway enrichment analysis showed that the expression of differential genes was closely related to the 5'-adenosine monophosphate-activated protein kinase (AMPK) signaling pathway and that the expression of forkhead box O 1 (FoxO1) was significantly increased in the presence of BMSCs. Furthermore, we determined the expression levels of p-AMPK/AMPK and p-FoxO1/FoxO1 by western blot analysis. The expression of p-AMPK/AMPK was upregulated, whereas that of p-FoxO1/FoxO1 was downregulated upon coculturing with BMSCs. The AMPK-specific antagonist Compound C inhibited the downregulation of p-FoxO1/FoxO1 induced by the BMSC coculture. Furthermore, treatment with the specific FoxO1 antagonist AS1842856 reduced the inhibitory effects of BMSCs on cardiomyocyte hypertrophy in vivo and in vitro. Our present study demonstrates the inhibition of cardiomyocyte hypertrophy by BMSCs, which occurs partly through the AMPK-FoxO1 signaling pathway.

In Situ Preparation of Amphibious ZnO Quantum Dots with Blue Fluorescence Based on Hyperbranched Polymers and their Application in Bio-Imaging.

A new strategy for preparing amphibious ZnO quantum dots (QDs) with blue fluorescence within hyper-branched poly(ethylenimine)s (HPEI) was proposed in this paper. By changing [Zn2+]/[OH-] molar ratio and heating time, ZnO QDs with a quantum yields (QY) of 30% in ethanol were obtained. Benefiting from the amphibious property of HPEI, the ZnO/HPEI nanocomposites in ethanol could be dissolved in chloroform and water, acquiring a QY of 53%, chloroform and 11% in water. By this strategy, the ZnO/HPEI nano-composites could be applied in not only in optoelectronics, but also biomedical fields (such as bio-imaging and gene transfection). The bio-imaging application of water-soluble ZnO/HPEI nanocomposites was investigated and it was found that they could easily be endocytosed by the COS-7 cells, without transfection reagent, and they exhibited excellent biological imaging behavior.

Inhibition of COX2/PGD2-Related Autophagy Is Involved in the Mechanism of Brain Injury in T2DM Rat.

The present study was designed to observe the effect of COX2/PGD2-related autophagy on brain injury in type 2 diabetes rats. The histopathology was detected by haematoxylin-eosin staining. The learning and memory functions were evaluated by Morris water maze. The levels of insulin and PGD2 were measured by enzyme-linked immunosorbent assay. The expressions of COX2, p-AKT(S473), p-AMPK(T172), Aß, Beclin1, LC3BII, and p62 were measured by immunohistochemistry and Western blotting. In model rats, we found that the body weight was significantly decreased, the blood glucose levels were significantly increased, the plasma insulin content was significantly decreased, the learning and memory functions were impaired and the cortex and hippocampus neurons showed significant nuclear pyknosis. The levels of COX2, p-AKT(S473), PGD2, Aß, Beclin1 and p62 were significantly increased, whereas the expression of p-AMPK(T172) and LC3BII was significantly decreased in the cortex and hippocampus of model rats. In meloxicam-treated rats, the body weight, blood glucose and the content of plasma insulin did not significantly change, the learning and memory functions were improved and nuclear pyknosis was improved in the cortex and hippocampus neurons. The expression of p-AMPK(T172), Beclin1 and LC3BII was significantly increased, and the levels of COX2, p-AKT(S473), PGD2, Aß, and p62 were significantly decreased in the cortex and hippocampus of meloxicam-treated rats. Our results suggested that the inhibition of COX2/PGD2-related autophagy was involved in the mechanism of brain injury caused by type 2 diabetes in rats.

Changes in the levels of 12/15-lipoxygenase, apoptosis-related proteins and inflammatory factors in the cortex of diabetic rats and the neuroprotection of baicalein.

This study was designed to investigate the neuroprotective effects of baicalein and the effect of the cortical 12/15-lipoxygenase (12/15-LOX) pathway on diabetic cognitive dysfunction. Our results showed that spatial learning and memory ability, as well as cortex neurons, were significantly impaired after the onset of diabetes. The fasting blood glucose and random blood glucose levels in the model group were significantly higher than those in the normal group. The levels of TG and TC in the plasma of the model group were significantly increased, but there was no significant difference in the LDL level. The insulin content in the plasma of diabetic rats was significantly lower than that of the normal group. The levels of inflammatory factors and 12(S)-HETE were significantly increased in diabetic rats, as were the protein expression levels of cPLA2, 12/15-LOX, p38MAPK, phospho-p38MAPK, caspase-3, caspase-9 and Aß1-42; by contrast, protein expression of Bcl-2 was significantly decreased. Administration of baicalein was shown to improve the spatial learning and memory ability and significantly decrease the levels of inflammatory cytokines. However, baicalein did not significantly influence the levels of blood glucose, lipids or insulin in rats. Baicalein treatment significantly protected diabetes rats from neuron death; significantly attenuated the overexpression of cPLA2, 12/15-LOX, p38MAPK, phospho-p38MAPK, caspase-3, caspase-9 and Aß1-42; and upregulated the expression of Bcl-2. These findings suggest that baicalein improves the cognitive function of diabetic rats by directly acting in the brain rather than by regulating the levels of blood glucose, lipids or insulin. In addition, baicalein can protect rat cortical neurons from damage caused by diabetes via inhibiting the 12/15-LOX pathway and relieving inflammation and apoptosis of the central nervous system.

CREB/Wnt10b mediates the effect of COX-2 on promoting BMP9-induced osteogenic differentiation via reducing adipogenic differentiation in mesenchymal stem cells.

Bone morphogenetic protein 9 (BMP9) is one of the most potent osteogenic factors, which may be a potential candidate for bone tissue engineering. However, the osteogenic capacity of BMP9 still need to be further enhanced. In this study, we determined the effect of Wnt10b on BMP9-induced osteogenic differentiation in mesenchymal stem cell (MSCs) and the possible mechanism underlying this process. We introduced the polymerase chain reaction (PCR), Western blot analysis, histochemical stain, ectopic bone formation, and microcomputed tomography analysis to evaluate the effect of Wnt10b on BMP9-induced osteogenic differentiation. Meanwhile, PCR, Western blot analysis, chromatin immunoprecipitation, and immunoprecipitation were used to analyze the possible relationship between BMP9 and Wnt10b. We found that BMP9 upregulates Wnt10b in C3H10T1/2 cells. Wnt10b increases the osteogenic markers and bone formation induced by BMP9 in C3H10T1/2 cells, and silencing Wnt10b decreases these effects of BMP9. Meanwhile, Wnt10b enhances the level of phosphorylated Smad1/5/8 (p-Smad1/5/8) induced by BMP9, which can be reduced by silencing Wnt10b. On the contrary, Wnt10b inhibits adipogenic markers induced by BMP9, which can be decreased by silencing Wnt10b. Further analysis indicated that BMP9 upregulates cyclooxygenase-2 (COX-2) and phosphorylation of cAMP-responsive element binding (p-CREB) simultaneously. COX-2 potentiates the effect of BMP9 on increasing p-CREB and Wnt10b, while silencing COX-2 decreases these effects. p-CREB interacts with p-Smad1/5/8 to bind the promoter of Wnt10b in C3H10T1/2 cells. Our findings suggested that Wnt10b can promote BMP9-induced osteogenic differentiation in MSCs, which may be mediated through enhancing BMP/Smad signal and reducing adipogenic differentiation; BMP9 may upregulate Wnt10b via the COX-2/p-CREB-dependent manner.

Self-template synthesis of hollow ellipsoid Ni-Mn sulfides for supercapacitors, electrocatalytic oxidation of glucose and water treatment.

In this work, we have successfully developed a simple self-template route for preparation of hollow ellipsoid Ni-Mn sulfides. This route involves the synthesis of solid Ni-Mn ellipsoids via a chemical precipitation method. Then, using thioacetamide (TAA) as the sulfur source, the solid Ni-Mn ellipsoids can be easily converted to hollow ellipsoid Ni-Mn sulfides in ethanol via sulfidation reaction. The as-synthesized hollow ellipsoid Ni-Mn sulfides possess large specific surface areas and porous structures. Benefiting from these structural and compositional advantages, the electrochemical performance of the hollow ellipsoid Ni-Mn sulfides is studied. As expected, the hollow ellipsoid Ni-Mn sulfides show a high specific capacitance of 1636.8 F g-1 at 2.0 A g-1 and good cycling stability (only 4.9% loss after 4000 cycles) as electrode materials for supercapacitors. Furthermore, electrocatalytic oxidation of glucose based on the synthesized hollow ellipsoid Ni-Mn sulfides is also performed. The hollow ellipsoid Ni-Mn sulfides present high sensitivity and selectivity, good stability and a low detection limit (0.02 µM). In addition, the as-synthesized hollow ellipsoid Ni-Mn sulfides exhibit good ability to remove the Congo red dyes from water, which gives them potential application in water treatment. The current work makes a major contribution to the design and preparation of hollow metal sulfide structures, as well as their potential applications in supercapacitors, electrocatalytic oxidation of glucose and water treatment.

Amidoselenation and Amidotelluration of Alkenes using Oxygen as Terminal Oxidant.

A protocol has been established for oxygen-mediated amidoselenation and amidotelluration of alkenes under mild conditions. This method provides a simple route to a series of structurally diverse ß-amido selenides and ß-amido tellurides in moderate to high yields. The wide substrate scope, good functional group tolerance, ease of large-scale preparation and potential for product derivatization make this reaction attractive for the synthesis of nitrogen-, selenium- and tellurium-containing molecules.

Mesoporous hybrid NiOx-MnOx nanoprisms for flexible solid-state asymmetric supercapacitors.

Mesoporous hybrid NiOx-MnOx nanoprisms have been successfully prepared in this work. The synthesis process involves a facile solvothermal method for preparation of Ni-Mn precursor particles and a subsequent annealing treatment. These mesoporous hybrid NiOx-MnOx nanoprisms have a high surface area of 101.6 m(2) g(-1). When evaluated as electrode materials in supercapacitors, the as-prepared mesoporous hybrid NiOx-MnOx nanoprisms deliver a specific capacitance of 1218 F g(-1) at a current density of 2.0 A g(-1). More importantly, the mesoporous hybrid NiOx-MnOx nanoprisms were successfully used to construct flexible solid-state asymmetric supercapacitors. The device shows a specific capacitance of 149.1 mF cm(-2) at 2.0 mA cm(-2), a good cycling stability with only 2.9% loss of capacitance after 5000 charge-discharge cycles, and good mechanical flexibility under different bending angles. These results support the promising application of mesoporous hybrid NiOx-MnOx nanoprisms as advanced supercapacitor materials.

Ferulic acid inhibits proliferation and promotes apoptosis via blockage of PI3K/Akt pathway in osteosarcoma cell.

Ferulic acid, a ubiquitous phenolic acid abundant in corn, wheat and flax, has potent anti-tumor effect in various cancer cell lines. However, the anti-tumor effect of ferulic acid on osteosarcoma remains unclear. Therefore, we conduct current study to examine the effect of ferulic acid on osteosarcoma cells and explore the underlying mechanisms. In present study, ferulic acid inhibited proliferation and induced apoptosis in both 143B and MG63 osteosarcoma cells dose-dependently, indicated by MTT assay and Annexin V-FITC apoptosis detection. Additionally, ferulic acid induced G0/G1 phase arrest and down-regulated the expression of cell cycle-related protein, CDK 2, CDK 4, CDK 6, confirmed by flow cytometry assay and western blotting. Moreover, ferulic acid upregulated Bax, downregulated Bcl-2, and subsequently enhanced caspase-3 activity. More importantly, ferulic acid dose-dependently inhibited PI3K/Akt activation. Using adenoviruses expressing active Akt, the anti-proliferation and pro-apoptosis of ferulic acid were reverted. Our results demonstrated that ferulic acid might inhibit proliferation and induce apoptosis via inhibiting PI3K/Akt pathway in osteosarcoma cells. Ferulic acid is a novel therapeutic agent for osteosarcoma.

Comparison of NiS2 and α-NiS hollow spheres for supercapacitors, non-enzymatic glucose sensors and water treatment.

NiS2 hollow spheres are successfully prepared by a one-step template free method. Meanwhile, α-NiS hollow spheres can also be synthesized via the calcination of the pre-obtained NiS2 hollow spheres at 400 °C for 1 h in air. The electrochemical performances of the as-prepared NiS2 and α-NiS hollow sphere products are evaluated. When used for supercapacitors, compared with NiS2 hollow spheres, the α-NiS hollow sphere electrode shows a large specific capacitance of 717.3 F g(-1) at 0.6 A g(-1) and a good cycle life. Furthermore, NiS2 and α-NiS hollow spheres are successfully applied to fabricate non-enzymatic glucose sensors. In particular, the α-NiS hollow spheres exhibit good catalytic activity for the oxidation of glucose, a fast amperometric response time of less than 5 s, and the detection limit is estimated to be 0.08 µM. More importantly, compared with other normally co-existing interfering species, such as ascorbic acid, uric acid and dopamine, the electrode modified with α-NiS hollow spheres shows good selectivity. Moreover, the α-NiS hollow spheres also present good capacity to remove Congo red organic pollutants from wastewater by their surface adsorption ability.

Polydatin Restores Endothelium-Dependent Relaxation in Rat Aorta Rings Impaired by High Glucose: A Novel Insight into the PPARß-NO Signaling Pathway.

Polydatin, a natural component from Polygonum Cuspidatum, has important therapeutic effects on metabolic syndrome. A novel therapeutic strategy using polydatin to improve vascular function has recently been proposed to treat diabetes-related cardiovascular complications. However, the biological role and molecular basis of polydatin's action on vascular endothelial cells (VECs)-mediated vasodilatation under diabetes-related hyperglycemia condition remain elusive. The present study aimed to assess the contribution of polydatin in restoring endothelium-dependent relaxation and to determine the details of its underlying mechanism. By measuring endothelium-dependent relaxation, we found that acetylcholine-induced vasodilation was impaired by elevated glucose (55 mmol/L); however, polydatin (1, 3, 10 µmol/L) could restore the relaxation in a dose-dependent manner. Polydatin could also improve the histological damage to endothelial cells in the thoracic aorta. Polydatin's effects were mediated via promoting the expression of endothelial NO synthase (eNOS), enhancing eNOS activity and decreasing the inducible NOS (iNOS) level, finally resulting in a beneficial increase in NO release, which probably, at least in part, through activation of the PPARß signaling pathway. The results provided a novel insight into polydatin action, via PPARß-NO signaling pathways, in restoring endothelial function in high glucose conditions. The results also indicated the potential utility of polydatin to treat diabetes related cardiovascular diseases.

Mesoporous ZnS-NiS Nanocomposites for Nonenzymatic Electrochemical Glucose Sensors.

Mesoporous ZnS-NiS composites are prepared via ion- exchange reactions using ZnS as the precursor. The prepared mesoporous ZnS-NiS composite materials have large surface areas (137.9 m(2) g(-1)) compared with the ZnS precursor. More importantly, the application of these mesoporous ZnS-NiS composites as nonenzymatic glucose sensors was successfully explored. Electrochemical sensors based on mesoporous ZnS-NiS composites exhibit a high selectivity and a low detection limit (0.125 µm) toward the oxidation of glucose, which can mainly be attributed to the morphological characteristics of the mesoporous structure with high specific surface area and a rational composition of the two constituents. In addition, the mesoporous ZnS-NiS composites coated on the surface of electrodes can be used to modify the mass transport regime, and this alteration can, in favorable circumstances, facilitate the amperometric discrimination between species. These results suggest that such mesoporous ZnS-NiS composites are promising materials for nonenzymatic glucose sensors.

Curcumin attenuates cardiomyocyte hypertrophy induced by high glucose and insulin via the PPARγ/Akt/NO signaling pathway.

AIM: To investigate the potential effect of curcumin on cardiomyocyte hypertrophy and a possible mechanism involving the PPARγ/Akt/NO signaling pathway in diabetes. METHODS: The cardiomyocyte hypertrophy induced by high glucose (25.5mmol/L) and insulin (0.1µmol/L) (HGI) and the antihypertrophic effect of curcumin were evaluated in primary culture by measuring the cell surface area, protein content and atrial natriuretic factor (ANF) mRNA expression. The mRNA and protein expressions were assayed by reverse transcription PCR and Western blotting, whereas the NO concentration and endothelial NO synthase (eNOS) activity were determined using nitrate reduction and ELISA methods, respectively. RESULTS: The cardiomyocyte hypertrophy induced by HGI was characterized by increasing ANF mRNA expression, total protein content, and cell surface area, with downregulated mRNA and protein expressions of both PPARγ and Akt, which paralleled the declining eNOS mRNA expression, eNOS content, and NO concentration. The effects of HGI were inhibited by curcumin (1, 3, 10µmol/L) in a concentration-dependent manner. GW9662 (10µmol/L), a selective PPARγ antagonist, could abolish the effects of curcumin. LY294002 (20µmol/L), an Akt blocker, and N(G)-nitro-l-arginine-methyl ester (100µmol/L), a NOS inhibitor, could also diminish the effects of curcumin. CONCLUSIONS: The results suggested that curcumin supplementation can improve HGI-induced cardiomyocytes hypertrophy in vitro through the activation of PPARγ/Akt/NO signaling pathway.

NiS hollow spheres for high-performance supercapacitors and non-enzymatic glucose sensors.

α-NiS and ß-NiS hollow spheres were successfully synthesized via the Kirkendall effect under different hydrothermal conditions. The obtained α-NiS and ß-NiS hollow spheres were evaluated as electrode materials for supercapacitors. Importantly, the α-NiS hollow sphere electrode has a large specific capacitance (562.3 F g(-1) at 0.60 A g(-1)) and good cycling property (maintaining about 97.5% at 2.4 A g(-1) after 1000 cycles). Furthermore, the as-prepared α-NiS and ß-NiS hollow spheres were successfully applied to construct electrochemical glucose sensors. Especially, the α-NiS hollow spheres exhibit a good sensitivity (155 µA mM(-1) cm(-2)), low detection limit (0.125 µM), and a wide linear range.

Stimulated emission in GaN-based laser diodes far below the threshold region.

We identify that the stimulated emission of GaN laser diodes (LDs) emerges far below the traditionally recognized threshold from both optical and electrical experiments. Below the threshold, the linear-polarized stimulated emission has been the dominating part of overall emission and closely related to resonant cavity. Its intensity increases super linearly with current while that of spontaneous emission increases almost linearly. Moreover, the separation of quasi-Fermi levels of electrons and holes across the active region has already exceeded the photon emission energy, namely, realized the population-inversion.

In situ preparation of fluorescent CdTe quantum dots with small thiols and hyperbranched polymers as co-stabilizers.

A new strategy for in situ preparation of highly fluorescent CdTe quantum dots (QDs) with 3-mercaptopropionic acid (MPA) and hyperbranched poly(amidoamine)s (HPAMAM) as co-stabilizers was proposed in this paper. MPA and HPAMAM were added in turn to coordinate Cd2+. After adding NaHTe and further microwave irradiation, fluorescent CdTe QDs stabilized by MPA and HPAMAM were obtained. Such a strategy avoids the aftertreatment of thiol-stabilized QDs in their bioapplication and provides an opportunity for direct biomedical use of QDs due to the existence of biocompatible HPAMAM. The resulting CdTe QDs combine the mechanical, biocompatibility properties of HPAMAM and the optical, electrical properties of CdTe QDs together.

Ferric phosphate hydroxide microcrystals for highly efficient visible-light-driven photocatalysts.

Fe4(OH)3(PO4)3 microcrystals are successfully synthesized by a simple hydrothermal method. Due to a possible self-etching mechanism, different morphologies of Fe4(OH)3(PO4)3 microcrystals are obtained. Several reactions with different temperatures and times are performed to confirm the supposed self-etching mechanism. Moreover, as a result of their different micro/nanostructures, these microcrystals present different photocatalytic activities for visible-light-driven photodegragadation of methylene blue.