Acrylonitrile ; poisoning ; Adult ; Female ; Humans ; Male ; Middle Aged ; Young Adult

Adolescent ; Case-Control Studies ; Child ; Child, Preschool ; Heart Defects, Congenital ; blood ; immunology ; Humans ; Infant ; Lymphocyte Subsets ; Th1 Cells ; immunology ; Th2 Cells ; immunology

Objective:To investigate the mechanism of endoplasmic reticulum (ER) stress-induced chemoresistance to cisplatin in gastric cancer cells. Methods:ER stress models were established in both BGC823 and SGC7901 gastric cancer cells. The expression of GRP78, an ER stress marker, was examined by Western blot analysis. Moreover, whether ER stress can decrease the sensitivity of gastric cancer cells to cisplatin and activate P38 was explored by flow cytometry and Western blot analysis, respectively. Whether ER stress-induced chemoresistance to cisplatin can be abrogated by blocking P38 activity in gastric cancer was also elucidated using flow cytometry. Results:GRP78 protein expression markedly increased after treating BGC823 and SGC7901 gastric cancer cells with tunica-mycin (TM) or thapsigargin (TG) for 8, 16, and 24 h (P<0.05), compared with that in the group treated for 0 h. The apoptotic rates of TM-(or TG)-, cisplatin-, and TM (or TG) plus cisplatin-treated groups significantly increased (P<0.05) in both BGC823 and SGC7901 gastric cancer cells compared with the rate in the control group. The apoptotic rate of TM (or TG) plus cisplatin-treated group signifi-cantly decreased (P<0.05) in both BGC823 and SGC7901 gastric cancer cells compared with that of the cisplatin-treated group. Com-pared with the group treated for 0 h, phospho-P38 expression markedly increased after treating BGC823 and SGC7901 gastric cancer cells with TM (or TG) for 8, 16, and 24 h (P<0.05). No difference in P38 protein expression was observed between each group in both BGC823 and SGC7901 gastric cancer cells (P>0.05). Both P38 inhibitors, either SB203580 or PD169316, can inhibit the activation of P38. The inhibition of P38 activity can overcome ER stress-induced chemoresistance to cisplatin in gastric cancer cells (P<0.05). Con-clusion:ER stress can trigger the chemoresistance to cisplatin by activating P38 in gastric cancer cells.

Drugs, Chinese Herbal ; chemistry ; Humans ; Isoflavones ; isolation & purification ; pharmacology ; Phytoestrogens ; Plant Preparations ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Platelet Aggregation Inhibitors ; isolation & purification ; pharmacology ; Pueraria ; chemistry ; Scutellaria baicalensis ; chemistry

Objective: To study the influence of gallic acid (GA) on the migration of human gastric carcinoma SGC-7901 cells, and to explore its mechanism.Methods: The human gastric carcinoma SGC-7901 cells were cultured and divided into control group and 3.125, 6.250, 12.500, 25.000, 50.000,100.000 mg·L-1 GA groups. The inhibitory rates of proliferation of SGC-7901 cells in various groups were examined by MTT assay;the migration abilities of SGC-7901 cells in various groups were measured with scratch assay;the expression levels of vascular of endothelial growth factor (VEGF) in various groups were detected by immunocytochemistry.Results: Compared with control group, the inhibitory rates of proliferation of SGC-7901 cells in different doses of GA groups were significantly increased in a dose-dependent manner(F=59.451,P<0.01).Compared with control group, the wound healing rates in different doses of GA groups were significantly decreased (P<0.01).Compared with control group, the expression levels of VEGF protein in 12.500 and 25.000 mg· L-1 GA groups were decreased (P<0.05).Conclusion: GA could inhibit the proliferation and migration of SGC-7901 cells through down-regulating the expression levels of VEGF protein.

The object of this study is to preparate the berberine hydrochloride (BBH) resin compound with taste masking effect. We took the BBH as the model drug and Amberlite IRP69 as the drug carriers, uncovered the curve of solubility of BBH in different cosolvent with a certain range of temperature, and then used it to calculate the parameters during the preparation of the complex such as adding quantity of BBH and the reaction temperature. Afterwards, the characteristic and in vitro release experiments were studied to verify the formation and predict the in vivo release behavior of the complex. The results showed that in the condition of using 60% ethanol as a cosolvent and stirring at 50 ℃ for 1 h, the drug loading and drug availability of the complex are at about 35% and 64%, respectively, and has a better taste-masking effect. In this study, a method was provided for preparing a taste-masking preparation of BBH.

In order to affirm the cardioactive components in Fuzi, we identified a group of aminoalcohol- diterpenoid alkaloids in Fuzi using ultra high-performance liquid chromatography coupled with electrospray ionization mass spectrometer (UPLC-ESI-MS) method. Among a total of forty-one isolated ingredients, thirteen major aminoalcohol-diterpenoid alkaloids were identified by comparing their retention times and MS spectra with those of the reference substances. Moreover, Fuzi samples from different places of origin and with different processing methods were examined and their components displayed a pattern of high similarity, though the relative abundance varies probably due to their different processing methods. Furthermore, the cardiac effect of each identified alkaloid was individually evaluated using the isolated bullfrog heart perfusion experiment. Among the thirteen aminoalcohol diterpenoid alkaloids tested, six of them significantly enhanced the amplitude rates. Taken together, we affirm that the cardioactive components in Fuzi are aminoalcohol-diterpenoid alkaloids, shedding light on future studies of the mechanisms and development of these cardioactive compounds.
Aconitum ; chemistry ; Alkaloids ; chemistry ; Amino Alcohols ; chemistry ; Animals ; Cardiotonic Agents ; chemistry ; Chromatography, High Pressure Liquid ; Drugs, Chinese Herbal ; chemistry ; Heart ; drug effects ; In Vitro Techniques ; Plant Extracts ; chemistry ; Rana catesbeiana ; Spectrometry, Mass, Electrospray Ionization

OBJECTIVEThe aim of the present study is to explore the effects of exhaustive exercise-induced oxidative stress on the antioxidant capacity and diformability of rat red blood cells.

METHODSRats were divided into three group (n = 10): sedentary control (C), exhaustive running exercise (ERE) and moderate running exercise (MRE) groups. Animals in the ERE group started treadmill running at a speed of 20 m/min speed with a 5% gradient, and reached a speed of 25 m/min with gradient 15% in 20 min. Running was continued until exhaustion. MRE group rats running at a speed of 20 m/min with a 5% gradient for 40 min. The levels of free thiol in erythrocyte membrane protein, lipidperoxidation levels and membrane protein components were analyzed. The red blood cell deformability of different groups was also observed.

RESULTSThe results showed that red blood cells were damaged by severe oxidative stress and the anti-oxidative capacity decreased significantly under exhaustive exercise conditions. Besides, lipid peroxidation and protein sulfhydryl cross-link based clustering of membrane were found after exhaustive exercise, and polymers high molecular weight (HMW) was formed. The elongation index (EI) was found to decline significantly in the ERE group compared with the C and MRE groups under shear stress (control group, 0.41 +/- 0.01 at 3 Pa and 0.571 +/- 0.008 at 30 Pa; ERE group, 0.314 +/- 0.013 at 3 Pa and 0.534 +/- 0.009 at 30 Pa; P < 0.05 and P < 0.01, respectively).

CONCLUSIONThese exercise-induced oxidative injure result in a significant decrease in deformability of rat erythrocytes, which in turn leads to dysfunction in the microcirculatory.

Animals ; Disease Models, Animal ; Erythrocyte Deformability ; Fatigue ; metabolism ; physiopathology ; Male ; Oxidative Stress ; Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley

OBJECTIVEThe objective of this study is to investigate the influence of mechanical properties and sintering performance by adding 5% weight percentage aids to nano-compound zirconia toughened alumina (ZTA) ceramics.

METHODSMicrometer Al2O3 and nanometer ZrO2 (quality ratio 4:1) were used to get 55% volume percentage slurry. Magnesium oxide and titanium oxide were taken as aids which were 5% weight percentage of the Al2O3 and ZrO2 powder. Five groups (number 0, 1, 2, 3, 4 group) were divided according to different proportion of aids. After gel-casting, the porcelain pieces were sintered at 1150, 1200, 1300, 1400, 1450, 1500, 1600 degrees C for 2 hours. Static three-point flexure strength, line shrinkage, relative density were measured and scanning electron microscopy (SEM) was used to observe section.

RESULTSNumber 1 (MgO 1%, TiO2 4%) group had the highest bending strength. It was (401.78+/-19.50) MPa after sintering at 1600 degrees C for 2 hours and was higher than 0 group (380.64+/-44.50) MPa. Bending strength became lower than 0 group when MgO was more than 2% or more than that weight percentage of ZTA powder. When MgO content was higher than 2% or more than that weight percentage, there was no difference in relative density raising rate between each sintering assistants groups. When the sintering temperature was higher than 1200 degrees C, all groups showed obvious line-shrinkage and the groups which contained sintering assistants were all was higher than 0 group.

CONCLUSIONAdding MgO and TiO2 aids from 1% to 4% weight percentage of ZTA will promote fritting and increase ZTA nano-compound ceramics mechanical properties. Adding 2% MgO aids or more than that weight percent will has no obvious help to increase the relative density raising rate of ZTA nano-compound ceramics and will degrade the mechanical properties of ZTA nano-compound ceramics.

Aluminum Oxide ; Dental Porcelain ; Microscopy, Electron, Scanning ; Temperature ; Titanium ; Zirconium

OBJECTIVECleidocranial dysplasia (CCD) is a dominantly inherited skeletal dysplasia caused by mutations in the osteoblast-specific transcription factor-encoding gene, core binding factor α1 (CBFA1). Over 90 mutations in CBFA1 gene have been published to date in 500 independent cases of CCD, including missense mutations, deletions, insertions, frameshift, and splice mutations. However, mutational screening of the CBFA1 gene is still far from saturation, and more novel mutations will be identified to enrich the insights into the molecular basis for the pathogenesis of CCD. The aim of this study was to explore the clinical and image features and detect the mutations of CBFA1 gene in two CCD families.

METHODIn this study, the clinical features were investigated in two CCD families, radiological and CT examinations regarding osseous malformation were carried out over the entire body of these patients with CCD. Blood (2 ml) was drawn from all affected individuals, unaffected family members and one hundred unrelated normal controls, Genomic DNA was extracted from whole blood with PureGene DNA extraction kit and PCR was performed with eight pairs of PCR primers for exons 0 to 7 of the CBFA1 gene. The mutations of CBFA1 gene were screened in these two CCD families.

RESULT(1) The clinical features of patients with CCD include delayed closure of fontanelles, frontal bossing, dysplasia of clavicles, late tooth eruption, and other skeletal anomalies. X-ray and CT examination showed the bulging calvarium, patent fontanelles, wide cranial sutures, multiple Wormian bones, dental dysplasia or aplasia of clavicles. (2) Two mutations were identified, one is novel missense mutation (c.1259C > T[p.T420I]) in CBFA1 gene exon 7, other (c.577C > T[p.R193X]) was reported in Chinese cases with CCD for the first time.

CONCLUSION(1) The clinical and image features of patients in two CCD families include delayed closure of fontanelles, frontal bossing, dysplasia of clavicles, late tooth eruption, and other skeletal anomalies. (2) The T420I and R193X mutations of CBFA1 were reported, expanding the spectrum of CBFA1 mutations causing CCD.

Child ; Child, Preschool ; Cleidocranial Dysplasia ; genetics ; pathology ; Core Binding Factor Alpha 1 Subunit ; genetics ; DNA Mutational Analysis ; Exons ; Female ; Humans ; Male ; Mutation ; Pedigree ; Phenotype