Design of a Negative Temperature Coefficient Temperature Measurement System Based on a Resistance Ratio Model.

In this paper, a temperature measurement system with NTC (Negative Temperature Coefficient) thermistors was designed. An MCU (Micro Control Unit) primarily operates by converting the voltage value collected by an ADC (Analog-to-Digital Converter) into the resistance value. The temperature value is then calculated, and a DAC (Digital-to-Analog Converter) outputs a current of 4 to 20 mA that is linearly related to the temperature value. The nonlinear characteristics of NTC thermistors pose a challenging problem. The nonlinear characteristics of NTC thermistors were to a great extent solved by using a resistance ratio model. The high precision of the NTC thermistor is obtained by fitting it with the Hoge equation. The results of actual measurements suggest that each module works properly, and the temperature measurement accuracy of 0.067 °C in the range from -40 °C to 120 °C has been achieved. The uncertainty of the output current is analyzed and calculated with the uncertainty of 0.0014 mA. This type of system has broad potential applications in industry fields such as the petrochemical industry.

Balsam-pear-like rutile/anatase core/shell titania nanorod arrays for photoelectrochemical water splitting.

In this work, a solution combustion followed by dissolution in hydrogen peroxide is adopted to achieve a precursor for decorating anatase TiO2 nanosheets along single-crystalline rutile TiO2 nanorods, which achieves balsam-pear-like core/shell nanorod arrays with enhanced photoelectrochemical water splitting. The enhanced photoelectrochemical performance is attributed to the novel nanoarchitecture, which can simultaneously offer a high surface area, enhanced light-harvesting, a rutile/anatase junction for charge carrier separation and a conductive pathway for charge carrier collection. The photoanode design can also give hints to other functional materials.

Formation of Mn-Co-Ni-O Nanoceramic Microspheres Using In Situ Ink-Jet Printing: Sintering Process Effect on the Microstructure and Electrical Properties.

Mn-Co-Ni-O nanoceramic microspheres with high density, uniformity, and size tunability are successfully fabricated using in situ ink-jet printing and two step sintering (TSS) techniques. The microspheres, synthesized by an effective and facile reverse microemulsion method, consist of uncalcined Mn-Co-Ni-O nanocrystallines that show a well formed single tetragonal spinel phase and an average particle size distribution of ≈20 nm. The sintering behavior, microstructure, and electrical properties of the Mn-Co-Ni-O nanoceramic microspheres are systematically investigated and characterized. The results indicate that the sintered Mn-Co-Ni-O nanoceramic microspheres show high density and improved electrical properties. The highest R25 , B25/50 , Ea , and α25 values achieved at sintering temperature of 1150 °C are 4846.7 KΩ, 4320 K, 0.401 eV, and -5.24% K-1 , respectively for these Mn-Co-Ni-O nanoceramic microspheres. Furthermore, the formation mechanism of uncalcined Mn-Co-Ni-O nanocrystallines and an analysis of the TSS procedure of the nanoceramic microspheres are discussed.

Caspase 3 is involved in the apoptosis induced by triptolide in HK-2 cells.

Triptolide, a main active component extracted from the traditional Chinese herbal medicine, Tripterygium wilfordii Hook. f (TWHf), has been shown to possess potent immunosuppressive and anti-inflammatory properties. However, the toxicity of triptolide limits its clinical applications. Here we treated the human proximal tubular epithelial cell line HK-2 cells with triptolide in vitro and investigated its toxic effects. The cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for viability inhibition and annexin V/propidium iodide (PI) staining for apoptosis/necrosis. The activation of caspase 3 was analyzed by Western Blotting. MTT assay showed triptolide inhibited the viability of HK-2 cells in a time- and dose-dependent manner. Flow cytometry assay showed triptolide caused apoptosis rather than necrosis in HK-2 cells by staining with annexin V/PI. Furthermore, the increase of cleaved p17 fragment, an active form of caspase 3, was detected. These results suggested that triptolide is able to cause cytotoxicity on HK-2 cells, and the mechanism of which is associated with caspase 3.

Bismuth trioxide-tailored sintering temperature, microstructure and NTCR characteristics of Mn1.1Co1.5Fe0.4O4 ceramics.

Mn1.1Co1.5Fe0.4O4 ceramics with tailored sintering temperature, microstructure, and NTCR characteristics were prepared using Bi2O3 sintering additive by a solid-state reaction route. Densification and morphological characterization indicate that bismuth trioxide can play a critical role in the sintering process. The results reveal that the sintering temperature can be decreased significantly from 1200 °C to 1050 °C by using the appropriate content of Bi2O3 additive. The resistivity decreases first and then increases with increasing Bi2O3 content. The obtained B 25/50 value and ρ 25 ranges were 3647-3697 K, and 800-1075 Ω cm, respectively. Oxygen sorption theory can be used to illustrate the optimal thermal stability (ΔR/R 0 = 0.10%). Complex impedance analysis further elucidates that grain boundaries make a dominant contribution to the total resistance. The mechanisms of grain boundary conduction and relaxation behavior are systematically analyzed. These findings open up a window for the further advancement of NTC ceramics at lower sintering temperature.

Participation of cathepsin B in emodin-induced apoptosis in HK-2 Cells.

Emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) and rhein (4,5-dihydroxyanthraquinone-2-carboxyl acid) are two main active compounds in total rhubarb anthraquinones (TRAs), which showed nephrotoxicity in Sprague Dawley (S.D.) rats in our previous study. However, it is unknown yet whether emodin and rhein have cytotoxic effects on kidney. To address this issue, HK-2 cells, a human proximal tubular epithelial cell line, were treated with different concentrations of emodin or rhein, and cell viability and morphological changes were investigated. The ratio of hypodiploid cells and the activity of caspase 3 protease were also detected. Results showed that addition of emodin but not rhein at concentrations above 40microM for 24h reduced cell viability and induced apoptosis in HK-2 cells. Additionally, emodin at apoptosis-inducing concentrations caused expression of cathepsin B (CB) protein and activation of CB protease. Addition of CB inhibitor, CA-074, significantly attenuated the ratio of hypodiploid and apoptotic cells, partially blocked caspase 3 activation and inhibited reduction of cell viability induced by emodin. These data indicate that emodin possesses cytotoxic effects on HK-2 cells partially through induction of CB protein and activation of CB protease.

QtUCP-a program for determining unit-cell parameters in electron diffraction experiments using double-tilt and rotation-tilt holders.

A computer program, QtUCP, has been developed based on several well-established algorithms using GCC 4.0 and Qt 4.0 (Open Source Edition) under Debian GNU/Linux 4.0r0. It can determine the unit-cell parameters from an electron diffraction tilt series obtained from both double-tilt and rotation-tilt holders. In this approach, two or more primitive cells of the reciprocal lattice are determined from experimental data, in the meantime, the measurement errors of the tilt angles are checked and minimized. Subsequently, the derived primitive cells are converted into the reduced form and then transformed into the reduced direct primitive cell. Finally all the patterns are indexed and the least-squares refinement is employed to obtain the optimized results of the lattice parameters. Finally, two examples are given to show the application of the program, one is based on the experiment, the other is from the simulation.

Cytotoxic effects and pro-apoptotic mechanism of TBIDOM, a novel dehydroabietylamine derivative, on human hepatocellular carcinoma SMMC-7721 cells.

We have investigated the antiproliferative effects of TBIDOM (N-(4-(2,2,2-trifluoroethyl) benzylidene) (7-isopropyl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octahydrophenanthren-1-yl) meth-anamine) and have explored its possible mechanisms on human hepatocellular carcinoma SMMC-7721 cells. The proliferative status of cells treated with TBIDOM was measured by the colorimetric MTT assay. Cellular apoptosis was analysed using Hoechst 33342 staining and flow cytometry. Reduction of mitochondrial membrane potential (Delta psi(m)) was also detected by flow cytometry. Western blotting assay was used to evaluate the release of cytochrome c and expression of p53, Bcl-2 and Bax proteins. It was shown that TBIDOM displayed a significant inhibitory effect on growth of SMMC-7721 cells in a dose- and time-dependent manner. Hoechst 33342 staining and flow cytometry analysis showed an increase of apoptosis rate and decrease of mitochondrial membrane potential after SMMC-7721 cells were exposed to TBIDOM for 24 h. Pretreatment of SMMC-7721 cells with TBIDOM significantly induced a decrease of Bcl-2 protein expression and an increase of caspase-3 activity and Bax protein expression. The results indicated that TBIDOM could effectively inhibit proliferation by induction of apoptosis and could be a promising candidate in the development of a novel class of antitumour agent.

[Chaihu Longgu Muli decoction combined with acupuncture at back-shu points for chronic fatigue syndrome].

OBJECTIVE: To observe the effect difference between Chaihu Longgu Muli decoction combined with acupuncture at back-shu points and simple Chaihu Longgu Muli decoction for chronic fatigue syndrome. METHODS: Sixty patients were randomly assigned into an herbal group and a combination group, 30 cases in each one. Simple Chaihu Longgu Muli decoction was used in the herbal group for continuous one month, one decoction a day. Based on that in the herbal group, 30 min acupuncture was used in the combination group at bilateral Xinshu (BL 15), Feishu (BL 13), Pishu (BL 20), Ganshu (BL 18) and Shenshu (BL 23), with acupoints according to syndrome differentiation. Acupuncture was given for 3 courses, 10 times as a course with 3 days between two courses, once a day. Fatigue status was evaluated before and after treatment by fatigue scale 14 (FS-14) and self-rating anxiety scale (SAS). RESULTS: The FS-14 scores, including body fatigue scores, mental fatigue scores and total scores, and SAS scores after treatment were lower than those before treatment in the two groups (all P<0.01), with better improvements in the combination group (all P<0.01). CONCLUSION: Chaihu Longgu Muli decoction combined with acupuncture at back-shu points can improve chronic fatigue syndrome, which are better than simple Chaihu Longgu Muli decoction.

Transactivation of the human NME5 gene by Sp1 in pancreatic cancer cells.

Non-metastatic cells 5 (NME5), a recently found gene belonging to the NDPK-like molecules gene family, is highly expressed in testis and some types of human cancer. Current studies have revealed diverse potential functions of NME5 and we have reported that NME5 is associated with innate resistance to gemcitabine in human pancreatic cancer cells in previous study. However, the mechanism underlying the transcriptional regulation of NME5 has not been elucidated yet. In this study, we analyzed the 5'-flanking region of the human NME5 gene and revealed its transcription start site (TSS) at -35 bp relative to its translation start codon ATG. Using 5' unidirectional deletion analysis, we demonstrated that the proximal promoter of NME5 is located within -1051 bp to +35 bp. Two functional GC-boxes (-300 bp and -323 bp) were identified within the promoter region. Mutation of either GC-box led to significant reduction in NME5 promoter activity, whereas overexpression of Sp1 activated NME5 promoter activity in MIA PaCa-2 and 293T cells. In silico analysis predicted that transcription factor Sp1 binds to both GC-boxes, which were confirmed by EMSA and ChIP. In addition, we found that compared with MIA PaCa-2, Sp1 was highly expressed in PAXC002, a well characterized human pancreatic cancer cell line with innate gemcitabine resistance where NME5 was reported to be highly expressed, indicating that Sp1 induces NEM5 expression in PAXC002 cells. In conclusion, our study characterized for the first time the human NME5 promoter which is controlled by Sp1 transcription factor in pancreatic cancer.

Rho kinase inhibitor Y-27632 down-regulates norepinephrine synthesis and release in PC12 cells.

Rho kinase inhibition is beneficial for neurite outgrowth and nerve disorders, and the Rho kinase inhibitors have been regarded as promising agents to treat neural diseases. The main aim of the study was to elucidate how Rho kinase inhibitor Y-27632 regulates neurotransmitter norepinephrine synthesis and release in PC12 cells when neurite outgrowth was induced. PC12 cells were treated with Y-27632 for 6 days. The amount of norepinephrine synthesized in PC12 cells and the amount released evoked by acetylcholine or by KCl were determined by norepinephrine enzyme-linked immunosorbent assay kits. The results showed that the amount of norepinephrine both synthesized and released was down-regulated with a concentration-dependent relationship. Further results of Western blotting found that the protein expression of tyrosine hydroxylase and synapsin I (especially its active form, synapsin I phosphoSer603) was also down-regulated, which were directly related to synthesis and release of norepinephrine, respectively. All the results suggest that Y-27632 is able to down-regulate norepinephrine synthesis and release, the direct mechanism of which may be associated with down-regulation on expression of some proteins, including tyrosine hydroxylase and synapsin I.

Effects of triptolide from Tripterygium wilfordii on ERalpha and p53 expression in two human breast cancer cell lines.

The aim of the study was to discover possible differential cytotoxicity of triptolide towards estrogen-sensitive MCF-7 versus estrogen-insensitive MDA-MB-231 human breast cancer cells. Considering that MCF-7 cells express functional Estrogen receptor alpha (ERalpha) and wild-type p53, whereas MDA-MB-231 cells which are ERalpha-negative express mutant p53, the anti-proliferation effect of triptolide on MCF-7 and MDA-MB-231 cells were examined, the apoptotic effect and cell cycle arrest caused by triptolide were investigated, ERalpha and p53 expression were also observed in this paper. The results showed that the anti-proliferation effects were induced by triptolide in both cell lines. But the value of IC(50) in MCF-7 cells for its anti-proliferation effect was about one tenth of that in MDA-MB-231 cells, which indicated that the effect is more potent in MCF-7 cells. Condensed chromatin or fragmented nuclei could be found in MCF-7 cells treated with only 40nM triptolide but in MDA-MB-231 cells they couldn't be observed until the concentration reached to 400nM. Triptolide induced significant S cell cycle arrest along with the presence of sub-G0/G1 peak in MDA-MB-231 cells, whereas there was only slightly S cell cycle arrest on cell cycle distribution in MCF-7 cells. The role of p53 in two breast cancer cells was examined, the results showed that the mutant p53 in MDA-MB-231 cells was suppressed and the wild-type p53 in MCF-7 was increased. Moreover, triptolide could down regulate the expression of ERalpha in MCF-7 cells. The results showed that triptolide is much more sensitive to ERalpha-positive MCF-7 cells than to ERalpha-negative MDA-MB-231 cells, and the sensitivity is significantly associated with the ERalpha and p53 status.

Involvement of mitochondrial pathway in triptolide-induced cytotoxicity in human normal liver L-02 cells.

Triptolide, a purified diterpenoid triepoxide compound derived from a traditional Chinese medicine, Tripterygium wilfordii HOOK. f (TWHf), has been used in the treatment of autoimmune and inflammatory diseases. However, the toxicity of triptolide limits its application to a great extent. In the present study, we treated human normal liver L-02 cells (L-02 cells) with triptolide in vitro and investigated its toxic effects. The cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for cellular viability and by flow cytometry and Hoechst 33258 staining for apoptosis. The mitochondrial membrane potential (delta psi m) was evaluated by flow cytometry with JC-1 as probe. After treatment with triptolide, a decrease in the viability of L-02 cells and increase in apoptosis were observed. Triptolide-induced apoptosis was accompanied by loss of mitochondrial membrane potential and release of cytochrome c (cyt-c) from the mitochondria to the cytosol and down-regulation of anti-apoptotic protein Bcl-2 levels with concurrent up-regulation in pro-apoptotic protein Bax levels and tumor suppressor protein p53 levels. Triptolide-increased activity of caspase 9 and caspase 3 was also observed. These results indicate that triptolide induced cytotoxicity in L-02 cells by apoptosis, which is mediated through mitochondrial pathway.

Simultaneous determination of triptolide, wilforlide A and triptonide in human plasma by high-performance liquid chromatography-electrospray ionization mass spectrometry.

A simple and sensitive method for the determination of triptolide, wilforlide A and triptonide in human plasma was developed and validated, using high-performance liquid chromatography-electrospray ionization mass spectrometry (LC-ESI-MS). Plasma samples were purified using solid-phase extraction (SPE) columns. The HPLC separation of the analytes was performed on a MACHEREY-NAGEL C(18)column (2.0 mm x 125 mm, 3 microm), using 2.7 mM formic acid containing 10 mM ammonium acetate-acetonitrile (55:45, v/v) as mobile phase, with a flow-rate of 0.25 ml/min. The compounds were ionized in the electrospray ionization (ESI) ion source of the mass spectrometer and were detected in the selected ion recording (SIR) mode. The calibration curves were linear in the 0.80-300 ng/ml range for all the three analytes, and the limits of detection were 0.25, 0.40, and 0.35 ng/ml for triptolide, wilforlide A, and triptonide, respectively. The average absolute recoveries for all the three analytes were above 81%. The methodology recoveries were greater than 91% and the relative standard deviations (RSD) of intra-day and inter-day were less than 15%. The developed method was successfully applied to the determination of triptolide, wilforlide A and triptonide concentration in patients' plasma after taking the medicament containing Tripterygium wilfordii HOOK. F.