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Hur, H,Kim, N K,Kim, H G,Min, B S,Lee, K Y,Shin, S J,Cheon, J H,Choi, S H Nature Publishing Group 2012 The British journal of cancer Vol.106 No.1
<P><B>Background:</B></P><P>This study aims to evaluate the effectiveness of adenosine triphosphate-based chemotherapy response assay (ATP-CRA)-guided neoadjuvant chemotherapy for increasing resectability in patients with unresectable colorectal liver metastasis.</P><P><B>Patients and methods:</B></P><P>Patients were randomised into two groups: Group A was treated by conventional chemotherapy regimen and Group B was treated by chemotherapy regimen according to the ATP-CRA. Three chemotherapeutic agents (5-fluorouracil, oxaliplatin and irinotecan) were tested by ATP-CRA and more sensitive agents were selected. Either FOLFOX or FOLFIRI was administered. Between Group A and B, treatment response and resectability were compared.</P><P><B>Results:</B></P><P>Between November 2008 and October 2010, a total 63 patients were randomised to Group A (<I>N</I>=32) or Group B (<I>N</I>=31). FOLFOX was more preferred in Group A than in Group B (26 out of 32 (81.3%) <I>vs</I> 20 out of 31 (64.5%)). Group B showed better treatment response than Group A (48.4% <I>vs</I> 21.9%, <I>P</I>=0.027). The resectability of hepatic lesion was higher in Group B (35.5% <I>vs</I> 12.5%, <I>P</I>=0.032). Mean duration from chemotherapy onset to the time of liver resection was 11 cycles (range 4–12) in Group A and 8 cycles (range 8–16) in Group B.</P><P><B>Conclusion:</B></P><P>This study showed that tailored-chemotherapy based on ATP-CRA could improve the treatment response and resectability in initially unresectable colorectal liver metastasis.</P>
Kim, E-K,Seo, H-S,Chae, M-J,Jeon, I-S,Song, B-Y,Park, Y-J,Ahn, H M,Yun, C-O,Kang, C-Y Macmillan Publishers Limited 2014 Gene therapy Vol.21 No.1
For successful clinical tumor immunotherapy outcomes, strong immune responses against tumor antigens must be generated. Cell-based vaccines compromise one strategy with which to induce appropriate strong immune responses. Previously, we established a natural killer T-cell (NKT) ligand-loaded, adenoviral vector-transduced B-cell-based anticancer cellular vaccine. To enhance tumor antigen delivery to B cells, we established a modified adenoviral vector (Ad-k35) that encoded a truncated form of the breast cancer antigen Her2/neu (Ad-k35HM) in which fiber structure was substituted with adenovirus serotype 35. We observed increased tumor antigen expression with Ad-k35HM in both human and murine B cells. In addition, an Ad-k35HM-transduced B-cell vaccine elicited strong antigen-specific cellular and humoral immune responses that were further enhanced with the additional loading of soluble NKT ligand KBC009. An Ad-k35HM-transduced, KBC009-loaded B-cell vaccine efficiently suppressed the in vivo growth of established tumors in a mouse model. Moreover, the vaccine elicited human leukocyte antigen (HLA)-A2 epitope-specific cytotoxic T-cell responses in B6.Cg (CB)-Tg (HLA-A/H2-D) 2Enge/Jat mice. These findings indicated that the Ad-k35 could be appropriate for the preclinical and clinical development of B-cell-based anticancer immunotherapies.
비정질 (Fe1-x Co x) 80 B20 합금의 결정화 과정에 대한 속도론적 연구
김택기,김윤배,오병현 대한금속재료학회(대한금속학회) 1985 대한금속·재료학회지 Vol.23 No.1
The thermal stability for the amorphous (Fe_(l-x)Co_x)_(80)B_(20) alloys has been studied systematically through DTA, X-ray diffraction pattern and the electrical resistance change response to temperature and time variations. The results obtained are as follows; 1) The crystallization temperature of amorphous (Fe_(l-x)Co_x)_(80)B_(20) alloy is independent of the concentration of Co and it is about 710˚K. 2) The crystallization process of amorphous (Fe_(l-x)Co_x)_(80)B_(20) alloy occurs in two steps; In the composition range of 0.1≤x≤0.5, amorphous (Fe_(l-x)Co_x)_(80)B_(20)→α phase (Fe, Co; bcc)+Fe₃B(bct) →α phase (Fe, Co; bcc)+Fe₂B(fct)+Co₂B(fct), and in the composition of x = 0.6 amorphous (Fe_(l-x)Co_x)_(80)B_(20)→α phase (Fe, Co; bcc) +Fe₃B(bct)+Co₃B(fct) →αphase (Fe, Co; bcc)+Fe₂B(fct)+Co₂B(fct), and in the composition of x = 0.7 amorphous (Fe_(l-x)Co_x)_(80)B_(20)→αphase (Fe, Co; bcc) +Co₃B(fco)→αphase (Fe, Co; bcc)+Fe₂B(fct)+Co₂B(fct) 3) The crystallization of amorphous (Fe_(l-x)Co_x)_(80)B_(20) is the diffusion-controlled nucleation and growth process, and the crystallization activation energy of amorphous (Fe_(l-x)Co_x)_(80)B_(20) alloy is independent of the composition of Co and it is about 70㎉/mole.
Hardening of Bi-Te based alloys by dispersing B<sub>4</sub>C nanoparticles
Jung, S.J.,Park, S.Y.,Kim, B.K.,Kwon, B.,Kim, S.K.,Park, H.H.,Kim, D.I.,Kim, J.Y.,Hyun, D.B.,Kim, J.S.,Baek, S.H. Elsevier Science 2015 Acta materialia Vol.97 No.-
Thermoelectric devices have attracted a great attention for renewable energy harvesters and solid-state coolers. For practical applications, the mechanical properties of thermoelectric materials become critical for the device reliability, a persistent performance with a long time and high operation cycles. Bi-Te based single-crystals, mostly used in commercial thermoelectric devices, are intrinsically brittle with weak van der Waals bonding, often leading to device failures such as crack and debonding during fabrication and operation. Thus, it is highly desirable to enhance the mechanical property of Bi-Te based alloys as well as the thermoelectric property. Here, we investigate the effect of B<SUB>4</SUB>C nanoparticles (less than 0.5wt%) dispersed in p-type Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> matrix on the mechanical properties. X-ray diffraction (XRD) result confirms that B<SUB>4</SUB>C-dispersed Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> has a single phase. We observe that the grain size of Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> becomes decreased with the B<SUB>4</SUB>C nanoparticle concentration by electron backscatter diffraction (EBSD) technique. Hardness, Young's modulus, and flexural strength of B<SUB>4</SUB>C-dispersed Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> are enhanced, compared to the B<SUB>4</SUB>C-free Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> polycrystals. On the other hand, the thermoelectric figure-of-merit of B<SUB>4</SUB>C-dispersed Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> is almost identical to that of the pure Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB>. Such enhancements of the mechanical properties of the B<SUB>4</SUB>C-dispersed Bi<SUB>0.4</SUB>Sb<SUB>1.6</SUB>Te<SUB>3</SUB> are attributed to the grain boundary hardening and second-phase hardening. Beyond thermoelectric materials, our result implies that the grain refinement by nanoparticle dispersion is a simple and promising way to strengthen the mechanical properties of other brittle materials with layered structure.
Genistein protects pancreatic β cells against cytokine-mediated toxicity
Kim, E.K.,Kwon, K.B.,Song, M.Y.,Seo, S.W.,Park, S.J.,Ka, S.O.,Na, L.,Kim, K.A.,Ryu, D.G.,So, H.S.,Park, R.,Park, J.W.,Park, B.H. North-Holland 2007 Molecular and cellular endocrinology Vol.278 No.1-2
In the past few decades, the use of genistein as an anti-inflammatory agent has gained much attention. Our current study focuses on the preventive effects of genistein on cytokine-induced pancreatic β-cell damage. Treatment of RINm5F (RIN) rat insulinoma cells with interleukin (IL)-1β and interferon (IFN)-γ induced cell damage, which was correlated with nitric oxide (NO) production. Genistein completely prevented cytokine-mediated cytotoxicity and NO production, a finding that correlated well with reduced levels of the inducible form of NO synthase (iNOS) mRNA and protein. The molecular mechanism of genistein inhibition of iNOS gene expression appeared to involve the inhibition of NFκB activation. The cytokine induced increases in NFκB binding activity, nuclear p50 and p65 subunit levels, and IκBα degradation in cytosol compared to unstimulated cells; genistein abolished all of these parameters. The cytoprotective effects of genistein are also mediated through the suppression of ERK-½ and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. In a second set of experiments, rat islets were used. The findings on β-cell protective effects of genistein were essentially the same as for the RIN cell data, namely genistein prevented cytokine-induced NO production, iNOS expression, ERK-½ activation, JAK/STAT activation, and impairment of glucose-stimulated insulin secretion. Collectively, these results suggest that genistein might be used to preserve functional β-cell mass.