[Platelet-rich Plasma Induces M2 Macrophage Polarization via Regulating AMPK Singling Pathway].

OBJECTIVE: To investigate the role of platelet-rich plasma (PRP) in inducing the M2 macrophage polarization via regulating AMPK singling pathway. METHODS: The expressions of M1 marker CD11c and M2 marker CD206 in macrophages of blank control group, LPS group, LPS+PRP group, and LPS+PRP+Compound C group were detected by flow cytometry. Western blot was used to observe the effects of PRP on the expression of AMPK-mTOR signaling pathway-related proteins at different times (12 h, 18 h and 24 h) after LPS treatment. RNA interference technology was used to silence the expression of AMPK in macrophages, and the expression of TGF-ß protein was subsequently examined by Western blot. RESULTS: LPS significantly reduced the expression of CD206 and increased the expression of CD11c (P <0.05). After the addition of PRP, the expression of CD206 was significantly increased (P <0.05), while the expression of CD11c was significantly decreased (P <0.05). Compared with LPS group, PRP treatment significantly increased the expressions of p-AMPK and p-ULK1 proteins at 12 h, 18 h and 24 h, while significantly decreased the expression of p-mTOR protein (P <0.05). After the addition of AMPK inhibitor Compound C, the expression of CD206 was significantly reduced (P <0.05) and the expression of CD11c was significantly increased compared with LPS+PRP group (P <0.05). After silencing the expression of AMPK in macrophages, the promotion effect of PRP on TGF-ß was significantly reduced (P <0.05). CONCLUSION: PRP can stimulate the transformation of macrophages to M2 type via AMPK signalling pathway.

A new type of phosphate-based phosphor Na3CsMg7(PO4)6:Eu2+/Mn2+ with high quantum efficiency and high thermostability.

The Eu2+ ion, with the 4f75d1 electronic configuration, is one of the most important activated ions due to its symmetry-allowed 4f → 5d electron transition. Herein, we successfully prepared a new type of blue phosphor, Na3CsMg7(PO4)6:xEu2+ (NCMP:xEu2+), in which Eu2+ occupies the Na+ sites of the host lattice. Under 395 nm light excitation, a broad emission band from 410 to 550 nm can be seen, peaking at 458 nm, due to the 5d → 4f transition of Eu2+. Moreover, Eu2+ can be used as a sensitizer ion in an NCMP host. For co-doping phosphor NCMP:0.18Eu2+/0.4Mn2+, both Eu2+ and Mn2+ emission bands can be seen using 395 nm as the excitation wavelength for the occurrence of Eu2+ → Mn2+ charge transfer. The optimized concentration of Eu2+ for NCMP:xEu2+ is x = 0.18, with high internal (IQE) and external quantum efficiencies (EQE) of 66.4% and 22.8%. The luminescence of NCMP:0.18Eu2+ has high thermostability with 77.3% the intensity at 450 K compared to that at 300 K. Finally, a white illuminating lamp was produced using a 395 nm UV chip, blue phosphor NCMP:xEu2+, green phosphor (Sr,Ba)2SiO4:Eu2+ and red phosphor CaAlSiN3:Eu2+ with CIE coordinates of (0.378, 0.369), color temperature (CCT) of 3971 K, and color rendering index (Ra) of 79.8.

Synthesis, crystal structure and luminescence properties of a new samarium borate phosphate, CsNa2Sm2(BO3)(PO4)2.

A new caesium sodium samarium borate phosphate, CsNa2Sm2(BO3)(PO4)2, has been obtained successfully by the high-temperature solution growth (HTSG) method and single-crystal X-ray diffraction analysis reveals that it crystallizes in the orthorhombic space group Cmcm. The structure contains BO3, PO4, NaO7 and SmO7 polyhedra which are interconnected via corner- or edge-sharing O atoms to form a three-dimensional [Na2Sm2(BO3)(PO4)2]∞ network. This network delimits large cavities where large Cs+ cations reside to form the total structure. Under 402 nm light excitation, CsNa2Sm2(BO3)(PO4)2 exhibits three emission bands due to the 4f→4f transitions of Sm3+. Furthermore, we introduced Gd3+ into Sm3+ sites to optimize the Sm3+ concentration and improve the luminescence intensity. The optimal concentration is Gd/Sm = 98/2. The luminescent lifetime of a series of CsNa2Gd2(1-x)Sm2x(BO3)(PO4)2 phosphors shows a gradual degradation of lifetime from 2.196 to 0.872 ms for x = 0.01-0.10. The Commission Internationale de l'Eclairage (CIE) 1931 calculation reveals that CsNa2Gd1.96Sm0.04(BO3)(PO4)2 can emit orange light under 402 nm excitation.

A novel stibium phosphate, LiBa(SbO)2(PO4)3: synthesis, crystal structure and RE3+-activated (RE = Tb3+ and Eu3+) fluorescence performance.

A new stibium phosphate, lithium barium bis(antimony oxide) tris(phosphate), LiBa(SbO)2(PO4)3, was prepared by the molten salt method with LiF as the flux. The crystal structure consists of an original three-dimensional anionic framework of [(SbO)2(PO4)3]∞ built from PO4 tetrahedra sharing their corners with SbO6 octahedra. This framework delimits one-dimensional tunnels where the lithium(I) and barium(II) ions are located. The UV-Vis spectrum shows that LiBa(SbO)2(PO4)3 was transparent from 350 to 800 nm, and is thus suitable as a luminescent host matrix. We then used Tb3+ and Eu3+ activators to test its luminous performance and the purities of the prepared phosphors were studied by powder X-ray diffraction analysis with Rietveld refinements. Photoluminescence (PL) studies reveal that the emission spectra of 1 mol% RE3+-doped (RE = Tb and Eu) samples can be excited by 371 and 394 nm light, emitting green and orange-red light, respectively, for Tb3+ and Eu3+. The CIE coordinates were measured to be (0.295, 0.571) and (0.6027, 0.3967), and the luminescent lifetimes were calculated as 0.178 and 1.159 ms, respectively.

Epigenetic silencing of miR-335 induces migration by targeting insulin-like growth factor-1 receptor in multiple myeloma.

Multiple myeloma (MM) is a common hematological malignancy and remains incurable. MiRNA-335 is a classic tumor suppressor, yet its expression pattern and biological role in MM is unclear. The aim of the present study was to determine the expression pattern, biological role, and mechanism of miR-335 in MM. In this study, we found that miR-335 expression was decreased in MM. The promoter of miR-335 was also hypermethylated in MM. It was found that over-expression of miR-335 or 5-azacytidine treatment suppressed migration of MM cells and down-regulated the expression of IGF-1R. MiR-335 thus acts as a metastatic suppressor by targeting IGF-1R in MM. Moreover, aberrant promoter hyper-methylation is critical for miR-335 silencing in MM. We also found that miR-335 assisted in predicting both the prognosis and progression of disease in MM patients. Observations might offer a new complementary diagnostic and therapeutic target in MM.

Enzymic degradation of hydroxyethyl cellulose and analysis of the substitution pattern along the polysaccharide chain.

The enzymatic degradation behavior of hydroxyethyl cellulose (HEC) samples with different molar substitutions (MS) values was investigated. The changes in the molecular structure of HEC treated with enzymatic approach in comparison to the native HEC were studied through nuclear magnetic resonance (NMR), fourier transform infrared spectra (FTIR), X-ray diffraction (XRD) and scanning electron microscopy (SEM) techniques and kinetics of degradation was studied by viscometry. The cleavage of HEC chains could be observed from FTIR and kinetics results. Moreover, reduce in molecular weight (Mw) of polymer and liberated glucose concentration was investigated by gel permeation chromatography (GPC) analysis during enzymatic degradation. And all these results indicated that HEC with lower MS is more susceptible to degrade and provided a better understanding of the mechanism operating during enzymatic hydrolysis of HEC by cellulases. Furthermore, by complete degradation and quantification of liberated glucose, the substitution index (SI) and the distribution of substituents along the HEC chain were investigated. The results suggested that the HEC samples differed in hydroxyethyl molar substitutions (MS) and possible distribution of the hydroxyethyl groups. Impressively, our efforts established a facile analytical method for the elucidation of the distribution of substituents along the HEC chain.

Effect of green tea on glucose control and insulin sensitivity: a meta-analysis of 17 randomized controlled trials.

BACKGROUND: The results of studies investigating the effect of green tea on glucose control and insulin sensitivity in humans are inconsistent. OBJECTIVE: We aimed to quantitatively evaluate the effect of green tea on glucose control and insulin sensitivity. DESIGN: We performed a strategic literature search of PubMed, EMBASE, and the Cochrane Library (updated to January 2013) for randomized controlled trials that evaluated the effects of green tea and green tea extract on glucose control and insulin sensitivity. Study quality was assessed by using the Jadad scale. Weighted mean differences were calculated for net changes in glycemic measures by using fixed-effects or random-effects models. We conducted prespecified subgroup and sensitivity analyses to explore potential heterogeneity. Meta-regression analyses were conducted to investigate dose effects of green tea on fasting glucose and insulin concentrations. RESULTS: Seventeen trials comprising a total of 1133 subjects were included in the current meta-analysis. Green tea consumption significantly reduced the fasting glucose and hemoglobin A1c (Hb A1c) concentrations by -0.09 mmol/L (95% CI: -0.15, -0.03 mmol/L; P < 0.01) and -0.30% (95% CI: -0.37, -0.22%; P < 0.01), respectively. Further stratified analyses from high Jadad score studies showed that green tea significantly reduced fasting insulin concentrations (-1.16 µIU/mL; 95% CI: -1.91, -0.40 µIU/mL; P = 0.03). CONCLUSIONS: This meta-analysis suggested that green tea had favorable effects, ie, decreased fasting glucose and Hb A1c concentrations. Subgroup analyses showed a significant reduction in fasting insulin concentrations in trials with high Jadad scores.

[MicroRNA expression profile and pathogenetic initial study in essential hypertension].

OBJECTIVE: To study the differential microRNAs expression between patients with essential hypertension and healthy controls. METHODS: Whole blood from 15 hypertensive patients and 5 controls healthies were separated into plasma at 3000 rpm for 10 minutes. MicroRNAs were harvested using kit, and stored at -80°C. MicroRNAs profiling were performed using Exiqon microRCURY(TM) LNA microRNAs array, and were quantitative RT-PCR for the differential microRNAs expression. In addition, we used a set of plasma samples from 24 hypertensive patients and 22 healthy donors to independently validate the expression of these signature microRNAs. RESULTS: MicroRNAs expression profile was found to be differentially in the essential hypertensive patients compared with the healthy donors. Of 1700 microRNAs detected on the microarray, 46 microRNAs were found to be differentially expressed in the essential hypertensive patient, 27 microRNAs were collected in Sanger microRNAs data-bank, the function of remaining 19 microRNAs were unknown. In the 27 microRNAs, 9 microRNAs were up-regulated in the hypertension patient samples, while 18 known microRNAs were down-regulated. MiR-296-5p (Fold change 0.47, P = 0.013) and miR-133b (Fold change 0.57, P = 0.033) were consistently down-regulated in the patient plasma, whereas let-7e (Fold change 1.62, P = 0.009) and hcmv-miR-UL112 (Fold change 2.72, P = 0.004), one human cytomegalovirus encoded microRNAs, were up-regulated in the patient samples. The microRNAs expression was independently validated using another sample. We showed that MHC class I polypeptide-related chain B (MHC class I polypeptide-related chain B, MICB) and Interferon regulatory factor 1 (Interferon regulatory factor 1, IRF1) were functional targets of hcmv-miR-UL112 by fluorescent reporter assays. CONCLUSIONS: The hypertensive patients have distinct microRNAs expression Profile. Hcmv-miR-UL112 may have important implications toward pathogenesis of essential hypertension.