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Kinetics Analysis (kinetics + analysis)
Selected AbstractsStimulatory effects of the soy phytoestrogen genistein on noradrenaline transporter and serotonin transporter activityMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 4 2010Yumiko Toyohira Abstract We examined the effects of genistein, one of the major soy phytoestrogens, on the activity of noradrenaline transporter (NAT) and serotonin transporter. Treatment with genistein (10,nM,10,,M) for 20,min stimulated [3H]noradrenaline (NA) uptake by SK-N-SH cells. Genistein also stimulated [3H]NA uptake and [3H]serotonin uptake by NAT and serotonin transporter transiently transfected COS-7 cells, respectively. Kinetics analysis of the effect of genistein on NAT activity in NAT-transfected COS-7 cells revealed that genistein significantly increased the maximal velocity of NA transport with little or no change in the affinity. Scatchard analysis of [3H]nisoxetine binding to NAT-transfected COS-7 cells showed that genistein increased the maximal binding without altering the dissociation constant. Although genistein is also known to be an inhibitor of tyrosine kinases, daidzein, another soy phytoestrogen and an inactive genistein analogue against tyrosine kinases, had little effect on [3H]NA uptake by SK-N-SH cells. The stimulatory effects on NAT activity were observed by treatment of tyrphostin 25, an inhibitor of epidermal growth factor receptor tyrosine kinase, whereas orthovanadate, a protein tyrosine phosphatase inhibitor, suppressed [3H]NA uptake by NAT-transfected COS-7 cells. These findings suggest that genistein up-regulates the activity of neuronal monoamine transporters probably through processes involving protein tyrosine phosphorylation. [source] Kinetics of esterification of palmitic acid with isopropanol using p -toluene sulfonic acid and zinc ethanoate supported over silica gel as catalystsJOURNAL OF CHEMICAL TECHNOLOGY & BIOTECHNOLOGY, Issue 10 2004Roomana Aafaqi Abstract Kinetic data on the esterification of palmitic acid with isopropanol were obtained using homogeneous (para -toluene sulfonic acid, p -TSA) and heterogeneous (zinc ethanoate coated on silica gel, ZnA/SG) catalysts in a batch reactor. The ZnA/SG catalyst was prepared using a sol,gel technique. The esterification reaction was studied at different reaction temperatures (373,443 K), initial reactants molar ratio (1,5), catalyst loading (1,5 gcat dm,3) and water concentration in feed (0,15 vol%). A power law rate equation was used for homogeneous kinetics analysis. The Langmuir Hinshelwood Hougen Watson (LHHW) model was used for heterogeneous kinetics. The kinetic parameters of both models were obtained using Polymath software. The reaction parameters were used to obtain simulated values of conversion for both catalytic systems. The simulated values were compared with the experimental values and were in good agreement. Copyright © 2004 Society of Chemical Industry [source] Epithelioid cell histiocytoma , histogenetic and kinetics analysis of dermal microvascular unit dendritic cell subpopulationsJOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2003Jeffrey S. Silverman Background:, Epithelioid cell histiocytoma (ECH), also known as epithelioid fibrous histiocytoma, is a peculiar dermal tumor, which can mimic melanocytic, vascular, epithelial, or other histiocytic lesions. Thought to arise from dermal dendrocytes, most ECH contain approximately 50% FXIIIa+ histiocytic dendrocytes, but not all lesional cells express FXIIIa. A putative fibroblastic component has not been characterized. Methods:, We analyzed the differentiation and cell kinetics of dermal microvascular unit cells in 12 previously reported ECH using antibodies to FXIIIa, CD68 (KP1), CD34, CD117, CD31, smooth muscle actin, collagen type 1 aminopropeptide, and MIB-1, using single and double immunostains. Results:, In ECH, many variably sized CD34/CD31+ tumor vessels with actin+ myopericytes were surrounded by epithelioid-to-dendritic cells of three types. About 5,80% were dendritic histiocytes that expressed FXIIIa but not CD31 or KP1. Fibroblasts, in some cases showing mild nuclear pleomorphism, were usually collagen type 1+, but CD34 and actin, in 11/12 cases. One ,early' ECH had 40% CD34+ epithelioid cells, admixed with 50% FXIIIa+ histiocytes. Most ECH had about 2,20% KP1+, CD117+ mast cells. Mast cell numbers increased with FXIIIa+ histiocyte numbers and the intensity of FXIIIa expression. MIB-1/FXIIIa double-labeling showed only rare cycling histiocytes, with numerous cycling fibroblasts and endothelial cells. Conclusions:, Our findings support the impression that ECH is a vascular fibrous histiocytoma. The constituent cells appear to arise from the activation of resident microvascular CD34+ dermal fibroblasts and the accumulation of FXIIIa+ dendritic stromal assembly histiocytes. The CD34+ cells appear to differentiate toward collagenous fibrocytes in association with histiocytes and mast cells in forming collagenous stroma and vessels. ECH is a tumor composed of all requisite cell types consistent with the origin from the dermal microvascular unit. [source] In-situ Polymerization of Rare-Earth Luminous PA6MACROMOLECULAR SYMPOSIA, Issue 1 2004Yumei Zhang Abstract Luminous polycaprolactam (PA6), synthesized through in-situ polymerization, is a composite of PA6 and uniformly dispersed luminous pigment. During the polymerization, it is found that as luminous pigment was added, the time of prepolycondensation was longer and the molecular weight increased by end-group analysis. It is also indicated that there was chemical coalescence between luminous pigment and PA6 through the end-group analysis and FTIR. From the results of DSC, it is shown that the luminous pigment had large effect on the crystal structure of the luminous PA6. The crystallinity of luminous PA6 varied with the content of the luminous pigment and the heat-treated conditions. From the crystallization kinetics analysis, it is shown that the crystallization rate of the composites increased as luminous pigment added. [source] Betulin induces mitochondrial cytochrome c release associated apoptosis in human cancer cellsMOLECULAR CARCINOGENESIS, Issue 7 2010Yang Li Abstract We examined whether betulin, a naturally abundant compound, has anticancer functions in human cancer cells. The results showed that betulin significantly inhibited cell viability in cervix carcinoma HeLa cells, hepatoma HepG2 cells, lung adenocarcinoma A549 cells, and breast cancer MCF-7 cells with IC50 values ranging from 10 to 15,µg/mL. While betulin exhibited only moderate anticancer activity in other human cancer cells such as hepatoma SK-HEP-1 cells, prostate carcinoma PC-3, and lung carcinoma NCI-H460, with IC50 values ranging from 20 to 60,µg/mL, it showed minor growth inhibition in human erythroleukemia K562 cells (IC50,>,100,µg/mL). We further investigated the mechanism of anticancer activity by betulin, using HeLa cells as an experimental model. Betulin (10,µg/mL) induces apoptotic cell death, as evidenced by morphological characteristics such as membrane phosphatidylserine translocation, nuclear condensation/fragmentation, and apoptotic body formation. A kinetics analysis showed that the depolarization of mitochondrial membrane potential and the release of mitochondrial cytochrome c occurred as early as 30,min after treatment with betulin. Betulin, unlike its chemical derivative betulinic acid, did not directly trigger mitochondrial cytochrome c release in isolated mitochondria. Importantly, Bax and Bak were rapidly translocated to the mitochondria 30,min after betulin treatment. The sequential activation of caspase-9 and caspase-3/-7 and the cleavage of poly(ADP-ribose) polymerase (PARP) were observed behind those mitochondrial events. Furthermore, specific downregulation of either caspase-9, Bax, or Bak by siRNA effectively reduced PARP cleavage and caspase-3 activation. Taken together, the lines of evidence demonstrate that betulin triggers apoptosis of human cancer cells through the intrinsic apoptotic pathway. © 2010 Wiley-Liss, Inc. [source] Hypoxia enhances proliferation of mouse embryonic stem cell-derived neural stem cellsBIOTECHNOLOGY & BIOENGINEERING, Issue 2 2010Carlos A.V. Rodrigues Abstract Neural stem (NS) cells can provide a source of material with potential applications for neural drug testing, developmental studies, or novel treatments for neurodegenerative diseases. Herein, the ex vivo expansion of a model system of mouse embryonic stem (mES) cell-derived NS cells was characterized and optimized, cells being cultivated under adherent conditions. Culture was first optimized in terms of initial cell plating density and oxygen concentration, known to strongly influence brain-derived NS cells. To this end, the growth of cells cultured under hypoxic (2%, 5%, and 10% O2) and normoxic (20% O2) conditions was compared. The results showed that 2,5% oxygen, without affecting multipotency, led to fold increase values in total cell number about twice higher than observed under 20% oxygen (20-fold vs. 10-fold, respectively) this effect being more pronounced when cells were plated at low density. With an optimal cell density of 104,cells/cm2, the maximum growth rates were 1.9,day,1 under hypoxia versus 1.7,day,1 under normoxia. Cell division kinetics analysis by flow cytometry based on PKH67 tracking showed that when cultured in hypoxia, cells are at least one divisional generation ahead compared to normoxia. In terms of cell cycle, a larger population in a quiescent G0 phase was observed in normoxic conditions. The optimization of NS cell culture performed here represents an important step toward the generation of a large number of neural cells from a reduced initial population, envisaging the potential application of these cells in multiple settings. Biotechnol. Bioeng. 2010;106: 260,270. © 2009 Wiley Periodicals, Inc. [source] Hydroxychloroquine potentiates Fas-mediated apoptosis of rheumatoid synoviocytesCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2006W.-U. Kim Summary Inadequate apoptosis may contribute to the synovial hyperplasia associated with rheumatoid arthritis (RA). The Fas-associated death domain protein (FADD)-like interleukin (IL)-1,-converting enzyme (FLICE)-inhibitory protein (FLIP), which is an apoptotic inhibitor, has been implicated in the resistance to Fas-mediated apoptosis of synoviocytes. This study investigated whether hydroxychloroquine (HCQ), an anti-rheumatic drug, induces the apoptosis of rheumatoid synoviocytes, and modulates the expression of FLIP. Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and were cultured with various concentrations of HCQ in the presence or absence of the IgM anti-Fas monoclonal antibodies (mAb) (CH11). Treatment with HCQ, ranging from 1 to 100 µM, induced the apoptosis of FLS in a dose- and time-dependent manner. The increase in synoviocytes apoptosis by HCQ was associated with caspase-3 activation. A combined treatment of HCQ and anti-Fas mAb increased FLS apoptosis and caspase-3 activity synergistically, compared with either anti-Fas mAb or HCQ alone. The Fas expression level in the FLS was not increased by the HCQ treatment, while the FLIP mRNA and protein levels were decreased rapidly by the HCQ treatment. Moreover, time kinetics analysis revealed that the decreased expression of FLIP by HCQ preceded the apoptotic event that was triggered by HCQ plus anti-Fas mAb. Taken together, HCQ increases the apoptosis of rheumatoid synoviocytes by activating caspase-3, and also sensitizes rheumatoid synoviocytes to Fas-mediated apoptosis. Our data suggest that HCQ may exert its anti-rheumatic effect in rheumatoid joints through these mechanisms. [source] | |||||||||||||