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- 검색키워드
- 저자 : Alok Kumar Dwivedi (검색결과 2 건)
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A Novel Additive Texturing of Stainless Steel 316 L Through Binder Jetting Additive Manufacturing
Suryank Dwivedi,Amit Rai Dixit,Alok Kumar Das,Akash Nag 한국정밀공학회 2023 International Journal of Precision Engineering and Vol.10 No.6
The current study introduces the novel additive micro-texturing through the binder jetting additive manufacturing technique to fabricate circular micro-textured stainless steel 316L parts. The topographical analysis shows that the sample is manufactured with periodic feature sizes less than 250 μm and within an error limit of 7.62% with high metallographic purity. The wettability study indicates hydrophilic wetting behavior with contact angles in the ranges of 85.7°–82.5° for deionized water and 50.2°–36.7° for Hank’s balanced salt solution. The surface free energy for the textured part (53.484 mN/m) is improved by 72% compared to the untextured part (31.054 mN/m), leading to enhanced hydrophilicity. Further, in the scratch analysis, the textured sample shows better features intactness.
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Arunkumar Arumugam,Ramadevi Subramani,Sushmita Bose Nandy,Daniel Terreros,Alok Kumar Dwivedi,Edward Saltzstein,Rajkumar Lakshmanaswamy 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Growth hormone receptor (GHR) plays a vital role in breast cancer chemoresistance and metastasis but the mechanism is not fully understood. We determined if GHR could be a potential therapeutic target for estrogen receptor negative (ER−ve) breast cancer, which are highly chemoresistant and metastatic. GHR was stably knocked down in ER-ve breast cancer cells and its effect on cell proliferation, metastatic behavior, and chemosensitivity to docetaxel (DT) was assessed. Microarray analysis was performed to identify potential GHR downstream targets involved in chemoresistance. GHR and ATP-binding cassette sub-family G member 2 (ABCG2) overexpression and knockdown studies were performed to investigate the mechanism of GHR-induced chemoresistance. Patient-derived xenografts was used to study the effect of GHR and ABCG2. Immunohistochemical data was used to determine the correlation between GHR, pAKT, pmTOR, and ABCG2 expressions. GHR silencing drastically reduced the chemoresistant and metastatic behavior of ER-ve breast cancer cells and also inhibited AKT/mTOR pathway. In contrast, activation, or overexpression of GHR increased chemoresistance and metastasis by increasing the expression and promoter activity, of ABCG2. Inhibition of JAK2/STAT5 signaling repressed GHR-induced ABCG2 promoter activity and expression. Further, ABCG2 knockdown significantly increased the chemosensitivity. Finally, patient-derived xenograft studies revealed the role of GHR in chemoresistance. Overall, these findings demonstrate that targeting GHR could be a novel therapeutic approach to overcome chemoresistance and associated metastasis in aggressive ER-ve breast cancers.
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