• Title/Summary/Keyword: cell-based microfluidic chip

Search Result 13, Processing Time 0.021 seconds

Fabrication of PDMS microlens for optical detection (광학적 검출을 위한 PDMS 마이크로렌즈의 제작)

  • Park, Se-Wan;Kim, Hyeon-Cheol;Chun, Kuk-Jin
    • Journal of the Institute of Electronics Engineers of Korea SD
    • /
    • v.46 no.4
    • /
    • pp.15-20
    • /
    • 2009
  • In a detection system based on laser light scattering, focusing an excitation laser beam into a focal point of a channel in a microfluidic chip is important for obtaining the highest excitation intensity, and consequently for obtaining a laser light scattering signal using a photodetector with a high efficiency. In this paper, we present a polydimethylsiloxane (PDMS) microfluidic chip consisting of an integrated PDMS microlens for cell detection based on laser light scattering. We fabricated PDMS microlens for optical detection system by simply putting down on PDMS chips. The PDMS microlens was fabricated by photoresist reflow and replica molding. This fabrication technique is simple and has an excellent property in terms of the microlens and a high-dimensional accuracy. The PDMS microlens integrated on the PDMS microfluidic chip has been verified to improve the laser intensity, and accordingly, the signal-to-noise ratio and sensitivity of laser light scattering detection for red blood cells(RBCs)

Preparation of Porous PLGA Microfibers Using Gelatin Porogen Based on a Glass Capillary Device (젤라틴 기공유도물질과 유리모세관 장치를 이용한 다공성 PLGA 미세섬유의 제조)

  • Kim, Chul Min;Kim, Gyu Man
    • Journal of the Korean Society for Precision Engineering
    • /
    • v.33 no.1
    • /
    • pp.63-67
    • /
    • 2016
  • We present a method of fabricating poly (lactic-co-glycolic acid) (PLGA) porous microfibers using a pore template. PLGA microfibers were synthesized using a glass capillary tube in a poly-(dimethylsiloxane) (PDMS) microfluidic chip. Gelatin solution was used as a porous template to prepare pores in microfibers. Two phases of PLGA solutions in different solvents-DMSO (dimethyl sulfoxide) and DCM (dichloromethane)-were used to control the porosity and strength of the porous microfibers. The porosity of the PLGA microfibers differed depending on the ratio of flow rates in the two phases. The porous structure was formed in a spiral shape on the microfiber. The porous structure of the microfiber is expected to improve transfer of oxygen and nutrients, which is important for cell viability in tissue engineering.

Elucidating molecular mechanisms of acquired resistance to BRAF inhibitors in melanoma using a microfluidic device and deep sequencing

  • Han, Jiyeon;Jung, Yeonjoo;Jun, Yukyung;Park, Sungsu;Lee, Sanghyuk
    • Genomics & Informatics
    • /
    • v.19 no.1
    • /
    • pp.2.1-2.10
    • /
    • 2021
  • BRAF inhibitors (e.g., vemurafenib) are widely used to treat metastatic melanoma with the BRAF V600E mutation. The initial response is often dramatic, but treatment resistance leads to disease progression in the majority of cases. Although secondary mutations in the mitogen-activated protein kinase signaling pathway are known to be responsible for this phenomenon, the molecular mechanisms governing acquired resistance are not known in more than half of patients. Here we report a genome- and transcriptome-wide study investigating the molecular mechanisms of acquired resistance to BRAF inhibitors. A microfluidic chip with a concentration gradient of vemurafenib was utilized to rapidly obtain therapy-resistant clones from two melanoma cell lines with the BRAF V600E mutation (A375 and SK-MEL-28). Exome and transcriptome data were produced from 13 resistant clones and analyzed to identify secondary mutations and gene expression changes. Various mechanisms, including phenotype switching and metabolic reprogramming, have been determined to contribute to resistance development differently for each clone. The roles of microphthalmia-associated transcription factor, the master transcription factor in melanocyte differentiation/dedifferentiation, were highlighted in terms of phenotype switching. Our study provides an omics-based comprehensive overview of the molecular mechanisms governing acquired resistance to BRAF inhibitor therapy.