Effects of ultrasound irradiation on the properties of apricot kernels during accelerated debitterizing.

In this paper, studies were conducted to investigate the effects of ultrasonically accelerated debitterizing on the physicochemical properties of apricot kernels, such as color, texture, oil content, protein characteristics and amino acids, with UV-Vis spectroscopy, synchronous fluorescence spectroscopy, circular dichroism, electrophoresis, environmental scanning electron microscopy, and thermal property analysis. The results indicate that the novel debitterizing technique has insignificant influences on the oil and protein contents of apricot kernels; meanwhile, the color, texture and activity of beta-glucosidase were substantially improved, greatly contributing to the quality modification and shortening the debitterizing time. In addition, ultrasound greatly influenced the amino acid contents and compositions, the fluorescence spectra and the thermal properties of the apricot kernel proteins. In a word, all these results greatly contribute to our understanding of the debitterizing mechanism mediated by ultrasound irradiation and further prove the feasibility of this novel debitterizing technique in the practical processing of apricot kernels.

A Microscale Linear Phased-Array Ultrasonic Transducer Based on PZT Ceramics.

In this paper, a microscale high-frequency ultrasonic transducer was prepared by combining traditional planar ultrasonic phased-array technology and micro processing technology. The piezoelectric ceramic material PZT was used as the functional material of the transducer. The number of the arrays was 72, the width of each array was 50 µm, the pitch of each array was 70 µm, and the length of each array was 3 mm. The PZT chip was finely ground to a thickness of 130 µm and could reach a frequency of 10 MHz. The experimental platform of micron-scale precision was set up for a beam-forming lateral sound field test and imaging experiment to validate the theoretical analysis. The echo imaging test showed that a mold with a feature size of about 400 µm could be imaged well.

Optimization of ultrasound parameters and its effect on the properties of the activity of beta-glucosidase in apricot kernels.

In this paper, ultrasound was used as an auxiliary tool to activate the activity of beta-glucosidase (beta-GC) in apricot kernels, and its parameters were optimized to evaluate the effects on the beta-GC activity with the response surface methodology (RSM), variables including ultrasonic time, temperature, power and frequency. The results indicate that the obtained quadratic regression model could simulate the actual conditions, and the optimum conditions were as follows: exposure time of 31 min, temperature 50 °C, power 225 W and frequency 28 kHz, and the activity of beta-GC achieved 3.64 × 105 U/g·apricot kernel (dry weight), having an increase of 34.67% compared to the untreated beta-GC. In addition, the changes of the beta-GC properties demonstrated that ultrasound did improve the activity of beta-GC by influencing the beta-GC's properties of fluorescence, circular dichroism, thermal property, etc. All these results would contribute to understand the mechanism of the rapid debitterizing of apricot kernels accelerated by ultrasound.

[The Mechanism of Combination using mTORC1/2 Inhibitor and Imatinib to Suppress Cell Proliferation of Ph +ALL Cell Line].

OBJECTIVES: To investigate the anti-leukemia effect and mechanism of mTORC1/2 inhibitor PP242 combined with imatinib (IM) on the proliferation of Ph+ acute lymphoblastic leukemia (ALL) cell line SUP-B15. METHODS: SUP-B15 cell line was treated with PP242, imatinib (IM), or PP242 plus IM for 72 h, IC50 values (the concentration of drug required to kill 50% of the cells) and the combination index (CI ) of synergistic cytotoxicity was determined using MTT methods. The expressions of PI3K/Akt/mTOR and apoptosis associated proteins were examined by Western blot test. RESULTS: The IC50 value of IM alone was (1.50±0.09) µmol/L, however, the IC50 values were (0.81±0.030) µmol/L, (0.36±0.140) µmol/L and (0.02±0.002) µmol/L combined with 20 nmol/L, 30 nmol/L and 50 nmol/L of PP242, and the CI values were 0.764, 0.545 and 0.507, indicating two drugs had highly synergistic effect on anti-proliferation in the SUP-B15 cell line. The expressions of p-Akt, p-4EBP1, p-elF4E, p-cAbl, p-mTOR and p-P70 were down-regulated significantly in a dose-dependent and time-dependent manner after PP242 treatment#.Compared with PP242 or IM alone, the down-regulation of PI3K/Akt/mTOR signaling pathway and the up-regulation of the apoptosis associated proteins (bax and cleaved caspase-3) were more significant in the combination of two drugs. CONCLUSION: The combination of IM and PP242 could increase the inhibition of PI3K/Akt/mTOR signaling pathway and apoptosis mediated by bax and caspase-3 in SUP-B15 cell line.

[Effects of curcumin on the recovery of hind limb function after spinal cord injury in rats and its mechamism].

OBJECTIVE: To investigate the effects of curcumin on motor function, and to explore the neuroprotective mechanism of curcumin after the spinal cord injury in rats. The study will theoretical and experimental evidence for curcumin's clinical treatment. METHODS: HI-0400 spinal cord impactor was used to prepare animal models of acute of spinal cord injury. One hundred and five clean and healthy rats were randomly divide into three groups:sham operation group (Sham) spinal cord injury group (SCI) and curcumin group (SCI+CUR). Intragastric administration was administrated after 30min of the spinal cord injury model, after 1 time a day, until the death. SCI+CUR group was intragastric administration with curcumin (100 mg/kg) of 0.5% carboxymethyl cellulose sodium, and Sham and SCI group were treated with the same dose of 0.5% carboxymethyl cellulose sodium. The motor function recovery of 3,7,14,21 and 28 days after spinal cord injury were evaluated by basso,beatlie,bresnahan (BBB) score. The spinal cord tissue and blood samples were collected at postoperative 12 h, 1 d, 3 d and 7 d respectively, NF-kappa B was detected by immunofluorescence, Bcl-2, Bax and Caspase-3 were detected by immunohistochemistry. The expression of Bcl-2 and Bax was detected by Elisa. RESULTS: The statistic difference of BBB score between SCI group and CUR group in 3 day was not statistically significant. It was found that the 7,14,21 and 28 days BBB score in CUR group were statistically significant higher than that in SCI group(P<0.05).The expression of inflammatory factor NF-kappa B appeared in 12 h after spinal cord injury, 1 day peaked and 3 days decreased. In SCI+CUR group, the expression of NF-kappa B at each time point was similar to the SCI group, and there was a difference between group SCI+CUR and SCI group in 1day.There was no obvious staining of Bax and Bcl-2 in Sham group. The staining of Caspase-3 and Bax in SCI+CUR group was significantly weaker than that in SCI group, while Bcl-2 was stronger. CONCLUSIONS: Curcumin can promote the recovery of hindlimb motor function after spinal cord injury in rats.The mechanism is through inhibition of NF-K B to prevent inflammation; And inhibition the expression of Bax and Caspase-3, and promotion the expression of Bcl-2 to prevent apoptosis, so as to accelerate the recovery of motor function in the rats after spinal cord injury.

Mitochondrial ferritin, a new target for inhibiting neuronal tumor cell proliferation.

Mitochondrial ferritin (FtMt) has a significant effect on the regulation of cytosolic and mitochondrial iron levels. However, because of the deficiency of iron regulatory elements (IRE) in FtMt's gene sequence, the exact function of FtMt remains unclear. In the present study, we found that FtMt dramatically inhibited SH-SY5Y cell proliferation and tumor growth in nude mice. Interestingly, excess FtMt did not adversely affect the development of drosophila. Additionally, we found that the expression of FtMt in human normal brain tissue was significantly higher than that of neuroblastoma, but not higher than that of neurospongioma. However, the expression of transferrin receptor 1 is completely opposite. We therefore hypothesized that increased expression of FtMt may negatively affect the vitality of neuronal tumor cells. Therefore, we further investigated the underlying mechanisms of FtMt's inhibitory effects on neuronal tumor cell proliferation. As expected, FtMt overexpression disturbed the iron homeostasis of tumor cells and significantly downregulated the expression of proliferating cell nuclear antigen. Moreover, FtMt affected cell cycle, causing G1/S arrest by modifying the expression of cyclinD1, cyclinE, Cdk2, Cdk4 and p21. Remarkably, FtMt strongly upregulated the expression of the tumor suppressors, p53 and N-myc downstream-regulated gene-1 (NDRG1), but dramatically decreased C-myc, N-myc and p-Rb levels. This study demonstrates for the first time a new role and mechanism for FtMt in the regulation of cell cycle. We thus propose FtMt as a new candidate target for inhibiting neuronal tumor cell proliferation. Appropriate regulation of FtMt expression may prevent tumor cell growth. Our study may provide a new strategy for neuronal cancer therapy.

[COX-2 inhibitor celecoxib can suppress the proliferation of FLT3-ITD positive acute myeloid leukemia cells with prominent down regulation of MEK/MCL-1 expression in vitro].

The purpose of this study was to investigate the effects of Celecoxib on the proliferation of the FLT3-ITD positive and negative acute myeloid leukemia cells and its mechanism. The proliferation inhibition effect of Celecoxib with different doses on the FLT3-ITD positive cells MV4-11 and the FLT3-ITD negative K562 cells was detected by CCK-8 method, the cell apoptosis was determined by flow cytometry, and the MEK, Mcl-1, pAKT expression was tested by Western blot. The results showed that Celecoxib inhibited the proliferation of both MV4-11 and K562 cells, but the IC50 for MV4-11 was (29.14 ± 2.4) µmol/L, which was significantly lower than that of K562 cells (39.84 ± 1.0) µmol/L (P < 0.05); The induced apoptosis rate of Celecoxib at 20-80 µmol/L on MV4-11 was not observed, but there was apparent influence on K562 at the same concentration. Western blot showed that Celecoxib down-regulated the expression of MEK and Mcl-1 but did not change the expression of pAKT obviously on MV4-11 cells, while the expression of Mcl-1 was reduced a little, but no obvious change were found in the expression of MEK and pAKT on K562 cells. It is concluded that the Celecoxib can inhibit the proliferation of FLT3-ITD positive AML cells distinctly, and the potential mechanism may be related to the inhibition of the MEK/Mcl-1 signaling pathway.

Intervention effects of nedaplatin and cisplatin on proliferation and apoptosis of human tumour cells in vitro.

OBJECTIVE: To study synergistic effects of nedaplatin and cisplatin on three human carcinoma cell lines (esophageal carcinoma cell line Eca-109, ovarian carcinoma Skov-3 and cervical carcinoma Hela). METHODS: Inhibition effects were evaluated by MTT assay and cell apoptosis was detected by flow cytometry. In addition, changes of Ki-67, Bax and Bcl-2 at mRNA and protein levels were quantified by RT-PCR and Western blotting. RESULTS: Growth inhibition in each cell lines was dose-dependent after exposure to nedaplatin or cisplatin alone. The interaction of the two drugs was synergistic at higher concentrations according to the median-effect principle. The inhibition rates with nedaplatin, cisplatin and combined treatment were 41.9±4.1%, 47.4±2.9%, 52.5±0.9%(Eca-109), 39.0±1.26%, 45.0±1.45% , 56.2±1.44% (Skov-3) and 44.8±2.11%, 46.9±0.99%, 56.6±1.83% (Hela) respectively, with increase in apoptosis. Compared with the nedaplatin or cisplatin alone treatment group, the combinative treatment group's Ki-67 and bcl-2 mRNA (protein) expression was decreased while that of Bax mRNA (protein) was increased. CONCLUSION: Compared to the effects of nedaplatin or cisplatin alone at high concentrations, combination of nedaplatin and cisplatin at low concentrations proved to be much more effective for inhibition of proliferation and the induction of apoptosis in the Eca-109, Skov-3 and Hela cell lines.