Mechanism Study of Ultrasonic Vibration-Assisted Microgroove Forming of Precise Hot-Pressed Optical Glass.

Microgroove structures with helical pitches in a wavelength level are increasingly required in optical areas. However, conventional manufacturing techniques generate relatively high stresses during pressing, resulting in poor precision when forming microgrooves. This paper reports on the mechanism of the ultrasonic vibration-assisted microgroove forming of precise hot-pressed optical glass. A finite element (FE) thermocompression model of the viscoelastic material was developed and the entire forming process was numerically simulated using coupled thermal-structural analysis. The analysis of several process parameters was carried out using orthogonal experiments, from which the optimum combination of parameters was selected. The glass thermoforming process is also assisted by ultrasonic vibration. The thermal and mechanical effects of vibration improved material flow and optimized forming results. The average maximum stress in the glass during the forming process was only 3.04 × 10-3 Mpa, while the maximum stress in the hot-pressing stage without ultrasound was 1.648 Mpa. The stress results showed that the material-forming stress is significantly reduced.

Mechanisms underlying the production of chemokine CXCL11 in the reaction of renal tubular epithelial cells with CD4+ and CD8+ T cells.

AIM: To study the release mechanism of C-X-C motif chemokine 11 (CXCL11) and other chemokines after the co-cultivation of CD4+ and CD8+ T cells with the renal tubular epithelial cells (RTEC) in the process of allograft renal transplantation rejection. METHODS: The Human CD4+, CD8+ T cells were obtained from the blood of volunteers and kidney transplantation (Ktx) patients, and co-cultured with renal tubular epithelial cells (RTEC) in vitro. RT-PCR was run for detecting the mRNA transcription of CXCL11, IFN-induced protein of 10 (CXCL10), and IL-6 in cells after RTEC was stimulated with IFN-γ or co-cultured with CD4+ and CD8+ T cells. The concentration of CXCL11, CXCL10 and IL-6 in the culture medium was detected by Multiplex Assay after RTEC was stimulated with IFN-γ or co-cultured with CD4+ and CD8+ T cells. IFN-γ receptor antibody was used for interfering with the above reaction and the blocking effect was observed. Western blot was used for protein expression analysis. Finally, we applied renal biopsies from kidney transplantation patients with and without rejection to verify the results of the above experiments by using RT-PCR and Western blot. RESULTS: The mRNA expression of CXCL11 and CXCL10 were significantly increased after RTEC was stimulated with IFN-γ or co-cultured with CD4+ and CD8+ T cells. Multiplex Assay showed that the concentration of CXCL11 and CXCL10 in the supernatant were significantly increased in a time-dependence fashion after stimulation RTEC by IFN-γ. Anti-IFN-γ receptor1 (anti-IFN-γR1) antibody could reduce the production of CXCL11 and CXCL10 in this situation. The concentration of CXCL11 and CXCL11 in the supernatant was significantly increased with a time-dependent effect after the co-culture of CD4+ and CD8+ T cells with RTEC. The anti-IFN-γR1 blocked this effect. Our study showed that the expression levels of CXCL11 and CXCL10 were upgraded in the biopsies of patients with renal transplant rejection comparatively to pre-transplant biopsies, both at mRNA and protein levels. CONCLUSIONS: RTEC and T cells can stimulate each other during the acute rejection of allogeneic kidney transplantation and secret CXCL11，CXCL10 and other chemokines. IFN-γ plays a key role in this process.

Taurine Supplementation Reverses Diabetes-Induced Podocytes Injury via Modulation of the CSE/TRPC6 Axis and Improvement of Mitochondrial Function.

BACKGROUND: The protective effects of taurine supplementation on diabetic kidney disease (DKD) have been defined, but the mechanisms are not quite clear yet. TRPC6 has been shown to function in the homeostasis of podocytes, but whether TRPC6-modulated mitochondrial dysfunctions participating in taurine-induced renal protection during diabetes are unclear. METHODS: A DKD model was constructed using streptozocin (STZ), and an immortalized mouse podocytes cell line MPC-5 was used. Renal histology and western blot were used to analyze the expression levels of certain proteins. Cell proliferation assays, apoptosis assays, calcium influx, and mitochondrial functions were evaluated. RESULTS: In this study, taurine intervention improved STZ-induced DKD injuries, while it decreased both 24-h urinary protein and podocytes apoptosis. In detail, this study showed that taurine treatment decreased mitochondrial ROS productions by suppressing calcium overload and improving mitochondrial respiratory functions. Furthermore, the upregulation of TRPC6 is partially responsible for the calcium overload during high glucose treatment, whereas taurine treatment inhibited TRPC6 expression and partially attenuated high glucose-induced podocytes injuries. In addition, we demonstrated that taurine could upregulate CSE expression and inhibits TRPC6 expression via promoting the synthesis of H2S. CONCLUSION: Our study reveals that taurine intervention could partially attenuate the lesions of DKD by modulating the CSE/TRPC6 axis.

Comparison of the effect of bone marrow cells infusion through the portal vein and inferior vena cava combined with short-term rapamycin on allogeneic islet grafts in diabetic rats.

AIMS/INTRODUCTION: The study aimed to compare the impact of allogeneic bone marrow cells (BMCs) infusion through the inferior vena cava (IVC) and portal vein (PV) combined with rapamycin on allogeneic islet grafts in diabetic rats. MATERIALS AND METHODS: Recipient diabetic Wistar rats were infused with islets from Sprague-Dawley rats through the PV. PKH26-labeled BMCs of Sprague-Dawley rats were infused to recipients through the PV or IVC, followed by administration of rapamycin for 4 days. Blood glucose level was measured to evaluate the survival time of the islets. Lymphocytes separated from blood, BMCs, thymus, liver, spleen and lymph node were analyzed by flow cytometry. The peripheral blood smear, BMCs smear and frozen sections of tissues were observed by a fluorescence microscope. RESULTS: The survival time of the islets was significantly prolonged by the BMCs infusion combined with rapamycin. The rats receiving BMCs infusion through the PV induced a significantly longer survival time of the islets, and increased mixed chimeras of allogeneic BMCs in the thymus, liver, spleen and lymph node compared with the rats receiving BMCs infusion through the IVC. The amount of the mixed chimeras on day 14 was lower than that on day 7 after islet transplantation. Furthermore, PV transplantation had significantly more mixed chimera than IVC transplantation in all analyzed organs or tissues. CONCLUSIONS: BMCs infusion combined with rapamycin prolongs the islets survival and induces mixed chimeras of BMCs. PV infusion of BMCs might be a more effective strategy than IVC infusion of BMCs.

[Rapid determination of 129 pesticide residues in vegetables and fruits by gas chromatography-triple quadrupole mass spectrometry].

An analytical method for the simultaneous determination of 129 pesticides in vegetables and fruits was established based on optimized QuEChERS with gas chromatography-triple quadrupole mass spectrometry (GC-MS/MS). The samples were extracted with acetonitrile (containing 1% (v/v) acetic acid), then the extracts were determined by GC-MS/MS in multireaction monitoring (MRM) mode after being cleaned up with mixed solid-phase dispersion, and the external standard method was applied to quantify the pesticides. The results showed that all the 129 pesticides had good linearity in certain ranges with the correlation coefficients ( r2) higher than 0. 98. The average recoveries of the most of 129 pesticides in different matrices were in the range of 66.2% - 124.7% at the spiked level of 10 micro g/kg, with relative standard deviations (RSDs) of 0.9% - 24.4%. The limits of quantification (LOQs) of the method were 0.03 - 16.7 micro g/kg. The results demonstrated that the developed method is simple, rapid, sensitive and high efficient for screening multiple pesticide residues in vegetables and fruits.

Dexamethasone suppresses DU145 cell proliferation and cell cycle through inhibition of the extracellular signal-regulated kinase 1/2 pathway and cyclin D1 expression.

AIM: To determine the mechanisms of glucocorticoids in inhibiting advanced prostate cancer growth. METHODS: The cell proliferation and cell cycle of prostate cancer DU145 cells following dexamethasone treatment were determined by proliferation assay and fluorescence-activated cell sorter. Western blot analysis was carried out to evaluate the effects of dexamethasone on phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and expression of cyclin D1 in DU145 cells with or without glucocorticoid receptor (GR) antagonist RU486. Reverse transcription-polymerase chain reaction verified the expression of GR mRNA in DU145 cells. RESULTS: Dexamethasone significantly inhibited DU145 cell proliferation at the G(0)/G(1) phase. Western blot analysis showed a dramatic reduction of ERK1/2 activity and cyclin D1 expression in dexamethasone-treated cells. The decreased phosphorylation of ERK1/2 in dexamethasone-treated cells was attenuated by GR blockade. Additionally, the effects of dexamethasone in inhibiting cyclin D1 expression were altered by GR blockade. CONCLUSION: Dexamethasone suppresses DU145 cell proliferation and cell cycle, and the underlying mechanisms are through the inhibition of phosphorylation of ERK1/2 and cyclin D1 expression. The inhibition of ERK1/2 phosphorylation and cyclin D1 expression is attenuated by GR blockade, suggesting that GR regulates ERK1/2 and cyclin D1 pathways. These observations suggest that dexamethasone has a potential clinical application in prostate cancer therapy.

[Induction of apoptosis by mifepristone in androgen-independent prostate cancer cell lines in vitro].

OBJECTIVE: To investigate the effects of mifepristone on cell proliferation of human androgen-independent prostate carcinoma cell lines DU-145, PC-3 in vitro and the possible mechanisms involved. METHODS: The A values of the prostate cancer cells DU-145 and PC-3 in each group with various concentrations (1, 10, 50, 100 micromol/L) of mifepristone at various time intervals (24-120 h) were detected with the colorimetric 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl tetrazolium bromide assay. The apoptosis rates of the DU-145 and PC-3 cells treated with 10 micromol/L of mifepristone for 24 h and 48 h were assessed by flow cytometry analysis technique. Immunohistochemical technique was used to determine the expression of bax, bcl-2 and vascular endothelial growth factor (VEGF) proteins after treatment with 10 micromol/L of mifepristone. RESULTS: The A values of the cancer cells treated with 1 micromol/L of mifepristone were similar to that of controls, while those of the cells treated with 10 micromol/L, 50 micromol/L and 100 micromol/L of mifepristone were significantly different from that of controls (P < 0.01). Mifepristone markedly inhibited cell proliferation of prostate cancer cells DU-145 and PC-3 on a dose- and time-depending manner. The apoptosis rates of 10 micromol/L mifepristone for DU-145 cell line at 24 h, 48 h were respectively 15.3%, 30.4% with flow cytometry method and then PC-3 cell line were respectively 22.2%, 32.0%. Immunohistochemical technique showed the expression of bcl-2 and VEGF in the DU-145 and PC-3 cells treated with 10 micromol/L of mifepristone were significantly decreased, and the expression of bax was increased. CONCLUSIONS: Mifepristone can induce apoptosis of androgen-independent prostate cancer cell lines DU-145 and PC-3 in vitro. The apoptosis effect is time-and-dose dependent. Mifepristone could initiate a cell death command via apoptotic pathways decreasing the expression of VEGF protein, downregulating the expression of bcl-2 protein and increasing the expression of bax protein.