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Carbon materials are widely used as anode on Li-ion battery (LIB). In particular, the effect of electrical conductivity (EC) on the anode is related to capacity and retention, which are important factors for LIB performance. However, the relationship between carbon properties and battery performance is still unclear. This uncertainty is due to the sp3 and sp2 bond states, the diversity of carbon like amorphous structures, and impurities. In this study, we investigate the structure-EC relationship from over 50 carbon samples. The carbon used was graphite, carbon nanotube (CNT), carbon black (CB), hetero atom doped carbon, and the ones synthesized by solution plasma. The carbon materials are evaluated by X-ray diffraction (XRD), Raman spectroscopy, Thermogravimetric analysis (TGA), Energy-dispersive X-ray spectroscopy (EDX), and four-point probe (FPP) measurement. The characterized values were extracted from the results and analyzed by Cluster analysis (CA) with JMP software. CA was used to classify how carbons are related to each other. The clusters were divided into 3 big groups according to the presence of 002 peak and the degree of defects. Some clusters have been shown high conductivity when they have high crystallinity. It was also found that the heteroatomic effect was higher than the crystallinity in the part showing low EC range. However overall correlation with EC is still unclear. This is because XRD and Raman can only provide information of symmetric or periodic structures rather than the effect of disorder or amorphous parts, sizes and shapes are not considered. Thus, analysis of shapes and sizes such as SEM and BET, and additional measurements related to amorphous structures may be helpful to clarifying the correlation. Figure 1

Background Carbon monoxide (CO) and nitric oxide (NO) each have unique roles for various inflammatory states, including inflammatory bone resorption. Although it is known that NO can induce the expression of the cytoprotective enzyme HO-1, there is no information as to whether the protective effect of CO requires NO production or whether CO must induce the expression of HO-1 to exert its functional effects. Methods Murine osteoblast cells, MC3T3E1 osteoblasts, were cultured for CO and NO-associated HO-1 experiments and were transfected with pcDNA 3, pcDNA 3-HO-1, control siRNA or HO-1 siRNA using Nucleofector. For cell death measurement, MTT and annexin V assays were used. We performed Western blotting to check the expressions of HO-1 and iNOs and measured the HO-1 enzyme activity. We also measured the amounts of nitrite and nitrate using Griess reagents. Results The increased expression of HO-1 is required for the protective effect of NO and a single treatment of CO can increase the expression of HO-1, and this is also important for the protective effect of CO in MC3T3E1 osteoblasts. CO as well as NO attenuates the TNF-α-induced apoptosis in osteoblasts. The anti-apoptotic effect of CO or NO is not mediated by cGMP, and CO has no effect on the release of NO. The inhibition of HO-1 with using the HO-1 inhibitor ZnPP or HO-1 siRNA resulted in a striking increase of apoptosis in the CO/TNF-α-treated cells. Furthermore, HO-1 overexpression showed resistance against the TNF-α-induced cytotoxicity in the MC3T3E1 osteoblasts. Conclusions There is a need for HO-1 expression to mediate the protection provided by exogenous CO or NO in osteoblasts.

The toxicity of thapsigargin, a selective inhibitor of endoplasmic reticular Ca 2+ -ATPase, was investigated in osteoblasts. We induced apoptosis in murine osteoblastic MC3T3E1 cells by exposure to the thapsigargin. Thapsigargin transiently increased the phosphotransferase activity of c-Jun N-terminal kinases1 (JNK1), which might in turn activate transcriptional activity of activation protein-1 (AP-1). We then prepared extracts from thapsigargin-treated MC3T3E1 cells and monitored cleavage of acetyl-YVAD-AMC and acetyl-DEVD-AMC, fluorogenic substrates for caspase 1-like and caspase 3-like proteases, respectively. Thapsigargin significantly increased the proteolytic activity of caspase 3-like proteases, but not the activity of caspase 1-like proteases. Furthermore, thapsigargin increased the transcriptional activity of nuclear factor-κB (NF-κB). These data suggest that thapsigargin-induced apoptosis in osteoblasts may be via activation of JNK1, caspase 3-like family proteases, and transcriptional factors including AP-1 and NF-κB.

Publisher Summary In biomedicine, the geometries of 3D objects are obtained in terms of slices such as computed tomography and magnetic resonance imaging. Much research efforts have been made on surface reconstruction from these sets of contours to visualize 3D objects. However, relatively few works have been made on constructing 3D finite element models from these contours. This chapter presents a new tetrahedral meshing algorithm from the series of medical images to construct reliable finite element meshes for biomechanical analysis. In this scheme the sectional contours extracted from medical images are grouped into correspondence pairs, and by the use of tiling and branching processes the side surfaces among sections are triangulated. At each section the domains enclosed by contours are also triangulated, and an advancing front method employing basic operators is used to construct tetrahedral elements for each object between two sections. Sample meshes are constructed from medical images to demonstrate the capability of the proposed algorithm.

The induction of interleukin-6 (IL-6), using a proinflammatory cytokine (tumor necrosis factor-alpha), was studied in a human osteoblast cell line (MG-63) in relation to p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB transcription factor. When added to MG-63 cells, tumor necrosis factor-alpha (TNF-alpha) had a stimulatory effect on the production of IL-6, and this elevation was significantly reduced by SB203580, a specific p38 MAPK inhibitor. In addition, the stimulation of IL-6 release was also reduced by pyrrolidine dithiocarbamate (PDTC) or NF-kappaB SN50, which has been reported to be a potent NF-kappaB inhibitor. Both the NF-kappaB inhibitors in the presence of SB203580 had a more inhibitory effect on IL-6 release. In this study, TNF-alpha stimulated NF-kappaB binding affinity as well as p38 MAP kinase activation, leading to the release of IL-6. However, the specific inhibitor of p38 MAPK, SB203580, had no effect on TNF-alpha-induced NF-kappaB activation and both NF-kappaB inhibitors failed to reduce the p38 MAPK activation in the TNF-alpha-stimulated osteoblasts. In addition, inhibition of p38 MAPK partially, but significantly, impaired TNF-alpha-regulated release of osteocalcin, an important differentiation marker in osteoblasts. These results strongly suggest that both p38 MAPK and NF-kappaB are required in TNF-alpha-induced IL-6 synthesis and that these two TNF-alpha-activated pathways can be primarily dissociated. Furthermore, p38 MAPK may play a significant role in differentiation in MG-63 cells.

surgery from 1986 to 1995. Premenopausal women were treated with adjuvant ovarian ablation by irradiation and postmenopausal women with adjuvant Tamoxifen for 5 years. Steroid receptors contents were determined prospectively by the classical biochemical DCC method, while HER2 gene amplification was determined retrospectively by CISH in 134 women whose archival paraffin tissue samples were retrieved. Results: One hundred and thirty four patients whose HER2 status was determined (66 premenopausal and 68 postmenopausal) of median age of 51 years (range 35−76), were followed for median 11.8 years (range 0.9−19). Eleven (8.21%) patients were node negative with grade 3 BC and 125 (93.28%) had 1−3 positive nodes irrespective of tumor grade. Median disease free interval was 12.3 years (95%CI 10–17.8); median BC specific survival (BCSS) was 16.2 years (95%CI 13-Inf) and overall survival (OS) was 15.2 years (95%CI 12.1-Inf). HER2 gene amplification (CISH+) were noted in 21 (15.67%), while 113 (84.33%) had no HER2 gene amplification (CISH−). There was no significant difference in the risk for disease relapse [HR 1.25 (95%CI 0.678–2.29), p = 0.489], death from BC [HR 1.21 (95%CI (0.608–2.42), p = 0.591], and death from any cause [1.19 (0.637–2.23), p = 0.590] between CISH+ and CISH− subgroup. Cox regression analysis showed that only ER-/PgR+ status was an independent favorable risk factor for BCSS [HR 8.29 (95%CI 1.14–60.24, Wald test p = 0.028)] and OS [HR 7.51 (95%CI 1.31–68.97, Wald test p = 0.0009)]. Comparison between premenopausal and postmenopausal subgroups with CISH+ BC showed a trend toward longer OS in premenopausal women (Log rank test c1= 3.302, p = 0.069), while the OS difference in CISH− group reached statistical significance in premenopausal women (Log rank test c1= 4.849, p = 0.028). However, there was no difference in BCSS between premenopausal and postmenopausal subgroups regardless of HER2 status. Conclusion: Our results did not show that positive HER2 status had a significant influence on disease outcome in early SR-positive breast cancer patients treated with adjuvant endocrine therapy only.