380 research outputs found
Uber die Azotierreaktion von kornigem Calciumcarbid, I : Azotierung von zuschlagfreiem Calciumcarbid
There has been gasometrically followed to high degrees of reaction (α) the progress of the reaction between a uniformly granulated calciumcarbide powder of technical origin and nitrogen gas at 1 atm. and at 1060°, 1080°, 1100°, and 1120℃, without addition of reaction promotor, calciumcyanamide being thereby formed according to CaC_2+N_2=CaCN_2+C. Assuming that the powder particles are all spheres of the same radius a=0.1mm, the experimental results were arranged to give the relation a^2l^2=2kt, where l=(a-r)/(a=1-(1-α)^1/3, r the radius of the unreacted carbide core at the time t, and 2k=-2.7×10^14exp (-117kcal/RT)cm^2/min. This formal parabolic time law for the sphere has been considered in the light of the theories of Jander and of Serin and Ellickson
Preoperative Computed Tomography-Derived Bone Densities in Hounsfield Units at Implant Sites Acquired Primary Stability
The purpose of this study was to evaluate preoperative CT-derived bone densities in Hounsfield units (HU) at implant sites that acquired primary stability, and to compare these values to the optimal bone densities proposed in the literature. Fifty-one patients, 18 males (37 implant sites) and 33 females (67 implant sites) between 2003 and 2010 were assessed. CT data for different jaw sections, regions, and operating procedures were compared using the Kruskal-Wallis test and Scheffe's test for multiple comparisons (P < 0.05). The mean bone density in the maxilla was significantly lower than that in the mandible (P < 0.05); the mean bone densities in the 4 jaw regions decreased in the following order: anterior mandible > anterior maxilla > posterior mandible > posterior maxilla. The bone densities assessed by HU fell into the range of optimal bone densities associated with acquired primary implant stability proposed in the literature
A Finite-dimensional Control Design for Parabolic Distributed Parameter Systems
A finite-dimensional discrete-time distribution controller is designed for a class of distributed parameter systems with control inputs in and/or on the body. The systems are described by a partial differential equation of parabolic type. The measured outputs of the system are assumed to be obtained through a finite number of point sensors located in and/or on the system. The proposed controller is a combination of a low-spillover distribution observer and a liner state feedback law. Sufficient conditions are given for the existence of the output regulation. A practical trade-off measure is also shown between the order of the controller and the sampling interval. The low-spillover distribution observer is realized on the basis of an accurate modeling of the system which is described in discrete time and contains a special feedforward pass. By using standard state variable techniques in the finite-dimensional control theory, it becomes possible for system designers to construct a state feedback distribution observer-regulator without troublesome preparations such as sensor allocation to avoid the observation spillover
Research and Development Work on Lithium-ion Batteries for Environmental Vehicles
Interest in electric vehicles (EVs) and hybrid electric vehicles (HEVs) has risen dramatically on account of environmental and energy concerns. The biggest issues that must be addressed in order to popularize these advanced vehicles are related to the battery.We have been promoting vigorous R&
D work on batteries for application to environmental vehicles since the beginning of the 1990s. Attention was focused on lithium-ion batteries early on as a fundamental solution to the critical issue mentioned above. The conclusion was reached that the development of those potentialities to their fullest extent would create completely new forms of value unobtainable with conventional batteries. As a result of extensive theoretical studies and many experimental demonstrations, we successfully showed ahead of others that those potentialities did in fact exist and could be achieved.This paper makes clear the various performance requirements of advanced batteries for EV or HEV application, focusing in particular on the critical aspects of the battery thermal design and construction for system stability. It also explains how the power output of the lithium-ion battery has been substantially improved for application to HEVs.
Document type: Articl
The chimeric antibody chLpMab-7 targeting human podoplanin suppresses pulmonary metastasis via ADCC and CDC rather than via its neutralizing activity
Podoplanin (PDPN/Aggrus/T1α) binds to C-type lectin-like receptor-2 (CLEC-2) and induces platelet aggregation. PDPN is associated with malignant progression, tumor metastasis, and poor prognosis in several types of cancer. Although many anti-human PDPN (hPDPN) monoclonal antibodies (mAbs), such as D2-40 and NZ-1, have been established, these epitopes are limited to the platelet aggregation-stimulating (PLAG) domain (amino acids 29-54) of hPDPN. Recently, we developed a novel mouse anti-hPDPN mAb, LpMab-7, which is more sensitive than D2-40 and NZ-1, using the Cancer-specific mAb (CasMab) method. The epitope of LpMab-7 was shown to be entirely different from that of NZ-1, a neutralizing mAb against the PLAG domain according to an inhibition assay and lectin microarray analysis. In the present study, we produced a mouse-human chimeric anti-hPDPN mAb, chLpMab-7. ChLpMab-7 showed high antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Furthermore, chLpMab-7 inhibited the growth of hPDPN-expressing tumors in vivo. Although chLpMab-7 recognizes a non-PLAG domain of hPDPN, it suppressed the hematogenous metastasis of hPDPN-expressing tumors. These results indicated that chLpMab-7 suppressed tumor development and hematogenous metastasis in a neutralization-independent manner. In conclusion, hPDPN shows promise as a target in the development of a novel antibody-based therapy
Fibrocytes activate fibroblasts by PDGF.
Fibrocytes, which are bone marrow-derived collagen-producing cells, were reported to play a role in the pathogenesis of pulmonary fibrosis. However, their function in pulmonary fibrosis is unclear. We analyzed their function compared with that of monocytes and localization in fibrotic tissues in patients with idiopathic pulmonary fibrosis (IPF). We compared the gene expression profile of monocyte-derived fibrocytes with that of monocytes by microarray analysis. Proliferation and differentiation into myofibroblasts were examined by 3H-thymidine incorporation assay and Western blotting. We measured the level of growth factors in the culture supernatant of fibrocytes by ELISA. The localization of fibrocytes in lung tissues of patients with IPF was determined by immunofluorescence staining. Compared with monocytes, fibrocytes had higher expression of extracellular matrix- and growth factor-encoding genes, including PDGF-B, FGF-2 and VEGF-B. Although fibrocytes did not proliferate in response to PDGF, co-culture of fibrocytes stimulated the growth of lung fibroblasts through the production of PDGF-BB. In the lung of IPF patients, CD45+Collagen-I+FSP-1+ cells, which have a similar phenotype to fibrocytes, were detected and co-stained with anti-PDGF antibody. This study suggested that fibrocytes function in pulmonary fibrosis partly by producing PDGF in the lungs of IPF patients
Chimeric Anti-PDPN Antibody ChLpMab-2
Human podoplanin (hPDPN ), a platelet aggregation‐inducing transmembrane glycoprotein, is expressed in different types of tumors, and it binds to C‐type lectin‐like receptor 2 (CLEC ‐2). The overexpression of hPDPN is involved in invasion and metastasis. Anti‐hPDPN monoclonal antibodies (mAbs) such as NZ ‐1 have shown antitumor and antimetastatic activities by binding to the platelet aggregation‐stimulating (PLAG ) domain of hPDPN . Recently, we developed a novel mouse anti‐hPDPN mAb, LpMab‐2, using the cancer‐specific mAb (CasMab) technology. In this study we developed chLpMab‐2, a human–mouse chimeric anti‐hPDPN antibody, derived from LpMab‐2. chLpMab‐2 was produced using fucosyltransferase 8‐knockout (KO ) Chinese hamster ovary (CHO )‐S cell lines. By flow cytometry, chLpMab‐2 reacted with hPDPN ‐expressing cancer cell lines including glioblastomas, mesotheliomas, and lung cancers. However, it showed low reaction with normal cell lines such as lymphatic endothelial and renal epithelial cells. Moreover, chLpMab‐2 exhibited high antibody‐dependent cellular cytotoxicity (ADCC ) against PDPN ‐expressing cells, despite its low complement‐dependent cytotoxicity. Furthermore, treatment with chLpMab‐2 abolished tumor growth in xenograft models of CHO /hPDPN , indicating that chLpMab‐2 suppressed tumor development via ADCC . In conclusion, chLpMab‐2 could be useful as a novel antibody‐based therapy against hPDPN ‐expressing tumors
Reg3 alpha and Reg3 beta Expressions Followed by JAK2/STAT3 Activation Play a Pivotal Role in the Acceleration of Liver Hypertrophy in a Rat ALPPS Model
To explore the underlying mechanism of rapid liver hypertrophy by liver partition in associating liver partition and portal vein ligation for staged hepatectomy (ALPPS), liver partition at different sites was investigated. Increased inflammatory cytokines owing to the liver partition have been reportedly responsible. If this were true, rapid liver hypertrophy should be achieved regardless of where the liver was split. A male Sprague-Dawley rat model was created, in which a liver split was placed inside the portal vein ligated lobe (PiLL), in addition to the ALPPS and portal vein ligation (PVL) models. Liver regeneration rate, inflammatory cytokine levels, activation status of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway and expressions of regenerating islet-derived (Reg)3 alpha and Reg3 beta were investigated. The liver regeneration rate was significantly higher in the ALPPS group than in the PiLL group, whereas inflammatory cytokine levels were nearly equal. Additional volume increase in ALPPS group over PVL and PiLL groups was JAK2/STAT3-dependent. Reg3 alpha and Reg3 beta expressions were observed only in the ALPPS group. An increase in inflammatory cytokines was not enough to describe the mechanism of rapid liver hypertrophy in ALPPS. Expressions of Reg3 alpha and Reg3 beta could play an important role in conjunction with an activation of the JAK2/STAT3 pathway
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