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Abstract In this research, asphalt composites were produced by mixing asphalt with silica extracted from rice husk, with a ratio of asphalt to silica of 1:0, 1:1.7 and 1:2, and calcined at 150 °C. Development of structures was characterized using Fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), scanning electron microscopy (SEM), followed by differential thermal analysis (DTA/TGA). The FTIR results showed the presence of Si-OH, C=O, and C-H functional groups, which were associated with asphaltene, carbon, and silica, according to the XRD analysis. The results obtained also indicated the significant effect of rice husk silica addition on phase transformation of asphaltene into silica and carbon, while asphaltene molecules were practically undetected. The presence of silica and carbon resulted in increased decomposition temperature of the sample. Based on these characteristics, the samples were considered as a roof material, suggesting their potential use as a substitute for lightweight steel roof devices.

The neuropathology of mild traumatic brain injury in humans resulting from exposure to explosive blast is poorly understood as this condition is rarely fatal. A large animal model may better reflect the injury patterns in humans. We investigated the effect of explosive blasts on the constrained head minimizing the effects of whole head motion. Anesthetized Yucatan minipigs, with body and head restrained, were placed in a 3-walled test structure and exposed to 1, 2, or 3 explosive blast shock waves of the same intensity. Axonal injury was studied 3 weeks to 8 months postblast using β-amyloid precursor protein immunohistochemistry. Injury was confined to the periventricular white matter as early as 3-5 weeks after exposure to a single blast. The pattern was also present at 8 months postblast. Animals exposed to 2 and 3 blasts had more axonal injury than those exposed to a single blast. Although such increases in axonal injury may relate to the longer postblast survival time, it may also be due to the increased number of blast exposures. It is possible that the injury observed is due to a condition akin to mild traumatic brain injury or subconcussive injury in humans, and that periventricular injury may have neuropsychiatric implications., (© 2020 American Association of Neuropathologists, Inc. All rights reserved.)

Mild traumatic brain injury (mTBI) is the signature injury in warfighters exposed to explosive blasts. The pathology underlying mTBI is poorly understood, as this condition is rarely fatal and thus postmortem brains are difficult to obtain for neuropathological studies. Here we report on studies of an experimental model with a gyrencephalic brain that is exposed to single and multiple explosive blast pressure waves. To determine injuries to the brain resulting from the primary blast, experimental conditions were controlled to eliminate any secondary or tertiary injury from blasts. We found small but significant levels of neuronal loss in the hippocampus, a brain area that is important for cognitive functions. Furthermore, neuronal loss increased with multiple blasts and the degree of neuronal injury worsened with time post-blast. This is consistent with our findings in the blast-exposed human brain based on magnetic resonance spectroscopic imaging. The studies on this experimental model thus confirm what has been presumed to be the case with the warfighter, namely that exposure to multiple blasts causes increased brain injury. Additionally, as in other studies of both explosive blast as well as closed head mTBI, we found astrocyte activation. Activated microglia were also prominent in white matter tracts, particularly in animals exposed to multiple blasts and at long post-blast intervals, even though injured axons (i.e. β-APP positive) were not found in these areas. Microglial activation appears to be a delayed response, though whether they may contribute to inflammation related injury mechanism at even longer post-blast times than we tested here, remains to be explored. Petechial hemorrhages or other gross signs of vascular injury were not observed in our study. These findings confirm the development of neuropathological changes due to blast exposure. The activation of astrocytes and microglia, cell types potentially involved in inflammatory processes, suggest an important area for future study.

This paper quantifies the mixing and dispersion from an outboard motor by field experiments in a small subtropical waterway. Organic dye was used as a surrogate for exhaust emissions and was mixed with uncontaminated creek water before being dispersed into the creek. Dye concentrations were measured with an array of concentration probes stationed in the creek. The data were then processed and fitted with a power law function. The corresponding dispersion constants agreed well with the literature. However, the amplitude was lower than the IMO equation but higher than the correlation from laboratory tests. Results for dye concentration intermittency (presence of dye) are presented for the first time from such field measurements and show significant mixing in-homogeneity., (Copyright © 2012. Published by Elsevier Ltd.)

Particle emissions, volatility, and the concentration of reactive oxygen species (ROS) were investigated for a pre-Euro I compression ignition engine to study the potential health impacts of employing ethanol fumigation technology. Engine testing was performed in two separate experimental campaigns with most testing performed at intermediate speed with four different load settings and various ethanol substitutions. A scanning mobility particle sizer (SMPS) was used to determine particle size distributions, a volatilization tandem differential mobility analyzer (V-TDMA) was used to explore particle volatility, and a new profluorescent nitroxide probe, BPEAnit, was used to investigate the potential toxicity of particles. The greatest particulate mass reduction was achieved with ethanol fumigation at full load, which contributed to the formation of a nucleation mode. Ethanol fumigation increased the volatility of particles by coating the particles with organic material or by making extra organic material available as an external mixture. In addition, the particle-related ROS concentrations increased with ethanol fumigation and were associated with the formation of a nucleation mode. The smaller particles, the increased volatility, and the increase in potential particle toxicity with ethanol fumigation may provide a substantial barrier for the uptake of fumigation technology using ethanol as a supplementary fuel.

In order to study the mechanism of the effect of heparin on apoptosis in carcinoma cells, the nasopharyngeal carcinoma cell line CNE2 was used to identify the effect of heparin on apoptosis associated with the expression of c-myc, bax, bcl-2 proteins by use of Hoechst 33258 staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), agarose gel electrophoresis, and flow cytometry, as well as Western blot analysis. The results showed that heparin induced apoptosis of CNE2 cells including the morphologic changes such as reduction in the volume, and the nuclear chromatin condensation, as well as the "ladder pattern" revealed by agarose gel electrophoresis of DNA in a concentration-dependent manner. The number of TUNEL-positive cells was dramatically increased to 33.6+/-1.2% from 2.8+/-0.3% by treatment with heparin in different concentrations (10 to approximately 40 kU/L). The apoptotic index was increased to 32.5% from 3.5% by detecting SubG1 peaks on flow cytometry. Western blot analysis showed that levels of bcl-2, bax and c-myc were significantly overexpressed by treatment with the increase of heparin concentrations. These results suggest that heparin induces apoptosis of CNE2 cells, which may be regulated by differential expression of apoptosis-related genes.

Objective: To study methods for blocking tumor metastasis., Methods: Endogenous laminin (LN), protein kinase C (PKC) inhibitor staurosporine (SP), anti-LN receptor (LN-R) were used to act on murine fibrosarcoma cells which were strongly positive for endogenous LN and LN-R, then infused into the caudal veins of 77 C57 mice once, to initiate lung tumor formation. Before infusion, the cells were all measured for surface LN-R quantity with flow cytometry., Results: The positive rate of LN-R on tumor cell surface in the control group, LN group, SP group, anti-LN-R group and anti-LN group being 56.5%, 76.3%, 50.2%, 31.9% and 20.6% respectively. The average volume of the tumors in the lungs of mice being 76 mm3, 110 mm3, 14 mm3, 5 mm3 and 20 mm3 respectively. The rate of tumor embolus formation in lymphatic and blood vessels being 81%, 94%, 36%, 43% and 68% respectively., Conclusion: The pathological changes and metastasis in the LN group are more svere than that in control group. But all other groups are less severe than the control group. The level of LN-R on tumor cell surface is positively correlated with tumor volume and rat of tumor embolus formation. The lipositol conduction system in tumor cells is also closely related with size of tumor foci and rate of tumor embolus formation.

Objective: To compare the variation in morphology of low and high metastatic variants C6 and C7, which were isolated from mouse lung adenocarcinoma cell line (LA795) by single cell culture technique., Method: The low and high metastatic variants C6 and C7 were used in vitro, to compare the variation in morphology, cytoskeleton, motility, adhesion under the action of LN molecule and to compare the variation in the expression of endogenous LN molecule as well., Results: Under LN molecule free culture condition, the motility and adhesion of high metastatic cell C6 were lower than those of low metastatic cells C7. This phenomenon indicated that the metastatic potential in vivo might be of negative correlation to the motility or adhesion in vitro. But if the LN molecules were added to the culture for 48 hours. Significantly, the motility and the adhesion were enhanced, the cytoskeleton network was reorganized, and the morphology was changed. In the C6 and C7 cells, both the motility and adhesion in vitro were positively correlated with the metastatic potential in vivo under the action of LN molecule. In addition, the distribution of the cytoskeleton network in the high metastatic variant C6 was uneven, irregular, close to one side of cell nucleus. The high metastatic cells C6 were shown strongly positive for endogenous LN by immunohistochemical technique and the distribution of the endogenous LN was close to one side of the cell nucleus., Conclusions: The quantity and distribution of endogenous and exogenous LN molecule and its receptors on the tumor cells may be an important factor for tumor metastatic heterogeneity. The mechanism of the action of LN molecule is correlated with the reorganization of the cytoskeleton.

Anti-bFGF serum was used to treat rabbit experimental silicosis. At 90 days, when experimental group was compared with control group, the number and size of the nodules in experimental group were much less and smaller than those in control group. Nodules in control group were mainly consist of fibroblast mixed with a small amount of collagen fiber, whereas nodules in experimental group were made up of macrophages. At 180 days, in addition to fibroblasts, there was II to III degree of collagen fiber in nodules of control group. Most of nodules in experimental group mainly contained macrophages. Fibroblasts of lung in fetal mice were cultured in vitro. The results showed that bFGF stimulated proliferation of fibroblast, whereas anti-bFGF serum inhibited fibroblast growth. It appeared that anti-bFGF serum actually blocked proliferation of fibroblast and fibrosis in rabbit experimental silicosis.

The current study shows that a clonal derivative of the Jurkat cell line up-regulates both the avidity and density of the alpha 6/beta 1 receptor in response to phorbol 12-myristate 13-acetate (PMA). This derivative attaches to fibronectin and, to a lesser degree, laminin constitutively. Adhesion and spreading are dramatically up-regulated following treatment with PMA. The response on fibronectin peaks within 4 hours, is insensitive to cyclohexamide, can be blocked by monoclonal antibodies (Mabs) to the beta 1 and alpha 5 subunits of the beta 1 family of integrins, and is not associated with increased expression of the alpha 5 or beta 1 epitopes at the cell surface. In contrast, the response on laminin is biphasic. The early phase parallels the response on fibronectin. The second phase peaks after 48-72 hours of treatment with PMA, is sensitive to cycloheximide, can be blocked by Mabs to the beta 1 and alpha 6 subunits, and is associated with increased expression of the alpha 6 epitope. Both the density independent and dependent responses to PMA in Jurkat cells are blocked by the protein kinase inhibitor staurosporine. The HSB-2, CEM, Molt-4, and HPB-ALL T-lymphoblastic cell lines also up-regulate attachment to fibronectin and laminin following treatment with PMA. All four lines constitutively attach to fibronectin and show rapid up-regulation of attachment following treatment with PMA. None of the lines attach to laminin prior to PMA treatment; however, specific adhesion developed after 4-120 hours of treatment. The most mature lines (Jurkat and HPB-ALL) up-regulated adhesion on laminin more rapidly than the less phenotypically mature lines (CEM, Molt-4, and HSB-2). In summary, clonal derivatives of the Jurkat cell line up-regulated attachment to laminin through protein kinase dependent increases in alpha 6/beta 1 receptor avidity and density. In addition, the expression of functional receptors for laminin is linked to developmental maturity in a series of T-lymphoblastic cell lines.

Human epidermal melanocytes were treated with all-trans-retinoic acid (RA) and examined for adhesion to bovine serum albumin-, fibronectin- and laminin-coated culture dishes. Control and treated cells were also examined for motility into micropore filters coated with the same proteins. Treatment of the cells with 3 x 10(-6) M RA for 3-4 days resulted in inhibition of attachment to all three substrates. Decreased attachment was observed within 1.5 h. Inhibition of attachment was not due to toxicity because differences between control and treated cells disappeared by 18 h, when most of the cells (approximately 75%) were attached and spread on all three substrates. The same treatment that inhibited adhesion also reduced migration into the interstices of micropore filters coated with the same three proteins. In additional experiments, human and mouse melanoma cell lines were examined in place of normal melanocytes. RA treatment also blocked adhesion and motility of these cells. The malignant melanoma cells were less sensitive to RA than normal melanocytes in the adhesion assay but were equally sensitive in the motility assay. The ability of RA to inhibit melanocyte adhesion and motility as well as melanocyte growth could explain, in part, the capacity of retinoids to modulate melanocyte function in hyperpigmented skin lesions.

Several variant cell lines that are deficient in surface laminin have been isolated from heterogeneous murine tumour populations. The parent populations from which these variant lines were isolated contain cells that express high levels of surface laminin as indicated by immunofluorescence, immunoperoxidase/electron microscopy and immunoprecipitation. The laminin-deficient lines were compared with their respective parent populations for motility by both the Boyden Chamber assay and the agarose assay. In both assays, the laminin-positive populations were much more motile than the laminin-deficient lines. The addition of exogenous laminin to the laminin-deficient lines significantly increased their motility. These observations are of interest since cell motility is thought to contribute to tumour cell metastasis, and the laminin-positive cell populations are highly tumorigenic and metastatic, while the laminin-deficient cells are of low tumorigenicity and are virtually non-metastatic.