Lattice Boltzmann simulation of the gas-solid adsorption process in reconstructed random porous media.

The gas-solid adsorption process in reconstructed random porous media is numerically studied with the lattice Boltzmann (LB) method at the pore scale with consideration of interparticle, interfacial, and intraparticle mass transfer performances. Adsorbent structures are reconstructed in two dimensions by employing the quartet structure generation set approach. To implement boundary conditions accurately, all the porous interfacial nodes are recognized and classified into 14 types using a proposed universal program called the boundary recognition and classification program. The multiple-relaxation-time LB model and single-relaxation-time LB model are adopted to simulate flow and mass transport, respectively. The interparticle, interfacial, and intraparticle mass transfer capacities are evaluated with the permeability factor and interparticle transfer coefficient, Langmuir adsorption kinetics, and the solid diffusion model, respectively. Adsorption processes are performed in two groups of adsorbent media with different porosities and particle sizes. External and internal mass transfer resistances govern the adsorption system. A large porosity leads to an early time for adsorption equilibrium because of the controlling factor of external resistance. External and internal resistances are dominant at small and large particle sizes, respectively. Particle size, under which the total resistance is minimum, ranges from 3 to 7 µm with the preset parameters. Pore-scale simulation clearly explains the effect of both external and internal mass transfer resistances. The present paper provides both theoretical and practical guidance for the design and optimization of adsorption systems.

Effects of transcranial direct current stimulation on hemichannel pannexin-1 and neural plasticity in rat model of cerebral infarction.

The aim of this study was to investigate the effects of transcranial direct current stimulation (TDCS) on hemichannel pannexin-1 (PX1) in cortical neurons and neural plasticity, and explore the optimal time window of TDCS therapy after stroke. Adult male Sprague-Dawley rats (n=90) were randomly assigned to sham operation, middle cerebral artery occlusion (MCAO), and TDCS groups, and underwent sham operation, unilateral middle cerebral artery (MCA) electrocoagulation, and unilateral MCA electrocoagulation plus TDCS (daily anodal and cathodal 10 Hz, 0.1 mA TDCS for 30 min beginning day 1 after stroke), respectively. Motor function was assessed using the beam walking test (BWT), and density of dendritic spines (DS) and PX1 mRNA expression were compared among groups on days 3, 7, and 14 after stroke. Effects of PX1 blockage on DS in hippocampal neurons after hypoxia-ischemia were observed. TDCS significantly improved motor function on days 7 and 14 after stroke as indicated by reduced BWT scores compared with the MCAO group. The density of DS was decreased after stroke; the TDCS group had increased DS density compared with the MCAO group on days 3, 7, and 14 (all P<0.0001). Cerebral infarction induced increased PX1 mRNA expression on days 3, 7, and 14 (P<0.0001), and the peak PX1 mRNA expression was observed on day 7. TDCS did not decrease the up-regulated PX1 mRNA expression after stroke on day 3, but did reduce the increased post-stroke PX1 mRNA expression on days 7 and 14 (P<0.0001). TDCS increased the DS density after stroke, indicating that it may promote neural plasticity after stroke. TDCS intervention from day 7 to day 14 after stroke demonstrated motor function improvement and can down-regulate the elevated PX1 mRNA expression after stroke.

A novel carbon nanotube structure formed in ultra-long nanochannels of anodic aluminum oxide templates.

We report the fabrication of a novel carbon structure consisting of uniform carbon nanotubes formed in the nanochannels of anodic aluminum oxide (AAO) templates, with the surface side open and connected by a uniform carbon sheet. The uniformity of the fabricated CNT arrays, plus the carbon film on the AAO surface interconnecting the open ends of all CNTs, constitute the major characteristics unique to our carbon structures. Some potential applications of such structures are noted.

1-Methyl-3-isobutylxanthine delays apoptosis induced by deprivation of growth factors in vascular endothelial cells.

AIM: To investigate the effects of 1-methyl-3-isobutylxanthine (MIBX) on apoptosis induced by deprivation of acidic fibroblast growth factor (aFGF) and serum in vascular endothelial cells (VEC). METHODS: Nuclear fragmentation was observed by fluorescence microscopy. Viability was determined by counting the cells that attached to dishes after treatments. DNA fragmentation was measured by agarose gel electrophoresis. RESULTS: The cells deprived of aFGF and serum were treated with MIBX 25-200 mumol/L for 3, 6, 9, and 12 h, respectively. Morphological changes including the formation of apoptotic bodies and DNA fragmentation of these cells were significantly suppressed by IBMX 50-200 mumol/L at 3 h and 6 h. But after 12-h treatment, no difference was observed between the treated and untreated cells. CONCLUSION: MIBX delays apoptosis of vascular endothelial cells induced by deprivation of aFGF and serum.

Involvement of gene expressions in apoptosis of vascular endothelial cells induced by rattlesnake venom.

Formation of apoptotic bodies is a typical character of apoptotic cell death, but how the processes are controlled is not known. In this study, we compared two apoptosis inducing systems in vascular endothelial cells (VEC). We found that the formation of apoptotic bodies during apoptosis induced by rattlesnake venom, which is an unique and specific apoptosis inducer to vascular endothelial cells, was much faster than that induced by deprivation of survival factors (aFGF and serum). When we blocked the synthesis of mRNAs in cells treated with rattlesnake venom by DRB (5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole), an inhibitor of transcription, the formation of apoptotic bodies was dramatically inhibited. We examined the expression of p53 gene and found that its expression was much higher in apoptosis induced by rattlesnake venom than that in apoptosis induced by deprivation of aFGF and serum. Our results suggest that gene expression is important and p53 gene may play a major role in inducing the formation of apoptotic bodies in VEC.

Effect of manoalide on apoptosis induced by deprivation of growth factors in vascular endothelial cells.

AIM: To study effect of manoalide on apoptosis induced by deprivation of acidic fibroblast growth factor (aFGF) and serum in vascular endothelial cells (VEC). METHODS: Morphologic changes were observed by light microscopy. Viability was determined by counting the cells that attached to dishes after treatments. DNA fragmentation was analyzed by agarose gel electrophoresis and fluorescence microscopy. RESULTS: The cells deprived of aFGF and serum were exposed to manoalide 1-4 mumol. L-1 for 48 h, detachment and DNA fragmentation of these cells were suppressed. At 7 mumol. L-1, manoalide promoted detachment and DNA fragmentation of VEC. CONCLUSION: manoalide 2 mumol.L-1 inhibited, but 7 mumol.L-1 promoted, apoptosis of VEC.

Integrin beta4 is involved in apoptotic signal transduction in endothelial cells.

To clarify the signal transduction in vascular endothelial cells (VEC) apoptosis induced by deprivation of FGF and serum, we investigated the function of integrin beta4 by using the monoclonal antibody (mAb) of this integrin. We added anti-beta 4 integrin mAb at the concentration of 5 microg/ml to the cells deprived of FGF and serum, apoptosis of these cells were completely inhibited 24 h after the treatment. Furthermore we plated the cells onto untreated bacterial culture plates on which the cells cannot adhere and spread in MCDB medium without FGF and serum; however, when anti-beta 4 integrin mAb was present at 5 microg/ml in the seeding medium, the cells rapidly adhered and spread. Our results first demonstrated that integrin beta4 participated in apoptotic signaling in VEC, and our findings indicate that hemidesmosome structures and keratin filament system might be important in regulation of apoptotic signaling.

Inhibitors of phospholipase promote apoptosis of human endothelial cells.

In order to understand the signal transduction system that regulates apoptosis of human umbilical vein endothelial cells (HUVEC), we investigated the effects of inhibitors of the activity of phospholipases. All three tested inhibitors of phospholipase A2 (PLA2), namely, manoalide, 3-(4-octadecyl)benzoylacrylic acid (OBAA), and oleyoxyethylphosphorylcholine (OOPC), induced apoptotic cell death of HUVEC. After 16 h of treatment, almost all of the cells had disintegrated into apoptotic bodies, and DNA ladders characteristic of apoptotic cell death were clearly observed upon analysis of DNA on agarose gels. The release of arachidonic acid from the cells that had been treated with manoalide, OBAA or OOPC (at the same concentrations as those at which these compounds induced apoptosis) was inhibited. We also studied the effects of two inhibitors of phosphatidylinositol-specific phospholipase C (PLC), U73122, and compound 48/80. Both compounds promoted the apoptosis of HUVEC. After 16 h of treatment, few cells remained intact, and DNA fragmentation was clearly detectable after only 12 h. Quantitation of inositol released from cells treated with U73122 and compound 48/80 showed that the release of inositol was blocked. By contrast, U73343, a similar aminosteroid that does not inactivate PLC, had no such effects. Our results suggest that PLA2 and phosphatidylinositol-specific PLC might be involved in the signaling pathway of apoptosis in HUVEC, and that the metabolism of arachidonic acid and of inositol might play important roles in the present apoptotic signal-transduction system.

Suppression of apoptosis by inhibition of phosphatidylcholine-specific phospholipase C in vascular endothelial cells.

In order to clarify the role of phosphatidylcholine-specific phospholipase C (PC-PLC) in the regulation of apoptosis in vascular endothelial cells (VEC), we investigated the effects of D609, a specific inhibitor of PC-PLC, on apoptosis that was induced by deprivation of fibroblast growth factor (FGF) and serum and also by rattlesnake venom. The early morphological changes (detachment of cells from dishes) and the fragmentation of DNA, which is a specific feature of apoptotic cell death, were clearly inhibited by D609 in these two apoptosis-inducing systems. Moreover, the production of diacylglycerol (DAG), which was stimulated in apoptotic VEC, was suppressed by D609. The effects of D609 on the activity of PC-PLC and on apoptosis of VEC were dose-dependent. Our results indicate that PC-PLC is involved in the apoptosis-inducing signal pathway in VEC and, that DAG, produced from phosphatidylcholine (PC), might be an important mediator in this signal-transduction pathway. Our results also suggest that rattlesnake venom, a strong promoter of apoptosis in VEC, might induce apoptosis by stimulating PC-PLC and, furthermore, that PC-PLC might play a significant role in anchorage-dependent signal transduction in VEC.

Relationships between phosphatidylcholine-specific phospholipase C and integrins in cell-substratum adhesion and apoptosis in vascular endothelial cells.

In order to understand the mechanism by which VEC control cell-substratum adhesion and apoptosis, we investigated relationships between PC-PLC and the integrins that are normally expressed in VEC. We found that promotion of cell-substratum adhesion by suppression of PC-PLC was almost completely blocked by a monoclonal antibody (mAb) against integrin beta1, and was partially blocked by a mAb against intergrin beta3. The production of diacylglycerol (DAG) which was inhibited by suppression of PC-PLC activity, was increased by mAbs against intergrin beta1 and beta3. When the mAb against integrin beta4 was added to the seeding medium, cell-substratum adhesion and spreading of cells were triggered, but the activity of PC-PLC was unaffected by this mAb. Furthermore, when both the mAb against integrin beta4 and a specific inhibitor (D609) of PC-PLC were present in the seeding medium, cell-substratum adhesion and spreading were promoted to a greater extent than when either of these agents was present alone. These data suggest that integrins beta1 and beta3 might regulate cell-substratum adhesion and apoptosis via a PC-PLC-dependent pathway, while integrin beta4 might regulate these phenomena via PC-PLC-independent pathway. These findings provide the first evidence of relationships between PC-PLC and integrins in cell-substratum adhesion and apoptosis.

Preliminary study on the microbiology of Campylobacter pyloridis and gastric histopathology.

Biopsy samples were taken endoscopically from the antral-mucosa of 693 patients with peptic ulcer and chronic gastritis presenting dyspepsia symptoms. Campylobacter pyloridis cultures were positive in 59 of 98 (60.2%) cases and histopathologically the organisms were found in 411 of 693 cases (59.3%). Pathologically, Campylobacter pyloridis was positive in 273 out of 300 patients with chronic superficial gastritis (91.0%), in 102 of 249 patients with chronic atrophic gastritis (40.9%), in 36 out of 144 patients with chronic atrophic gastritis with intestinalization or dysplasia (25.0%). We found that there was a significant association between the presence of Campylobacter pyloridis and chronic superficial gastritis, also the degree of lymphocyte infiltration showed a strong inverse association with the presence of Campylobacter pyloridis, suggesting that a local immune response might exert an important action in the eradication of this organism. These findings support the view that Campylobacter pyloridis, may be etiologically related to chronic gastritis and peptic ulceration, even though its role still remains to be determined.

[Cholesterol content and malignant proliferation of cancer cells].

The relationship between cholesterol content and proliferation of cancer cells was studied. When the cholesterol content of cancer cells increased. cAMP content of the cells also increased; the agglutinability of the cells decreased; the percentage of diploid cells increased greatly (from 54% to 79%) and the tetraploid cells reduced rapidly (from 43% to 15%). It was shown that the malignant proliferation of cancer cells decreased obviously. The cholesterol was not absorbed markedly by the V79 cell line and embryo lung cells as compared with the cancer cells when cholesterol content in the medium was increased. There were no apparent changes in the percentages of diploid cells or tetraploid cells.