Publications by authors named "Yohanes N S Nursalim"

Trophoblasts are placenta-specific epithelial cells that play an essential role in conducting nutrient, gas, and waste exchange between the fetus and the mother. Primary culture of human trophoblasts from donated term placentae is an important tool to study placental functions. Currently, there is a lack of general consensus of the optimal culture conditions for maintaining term trophoblast cells in vitro.

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The use of in vitro tools to study trophoblast differentiation and function is essential to improve understanding of normal and abnormal placental development. The relative accessibility of human placentae enables the use of primary trophoblasts and placental explants in a range of in vitro systems. Recent advances in stem cell models, three-dimensional organoid cultures, and organ-on-a-chip systems have further shed light on the complex microenvironment and cell-cell crosstalk involved in placental development.

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Extracellular vesicles (EVs) are emerging as key players in breast cancer progression and hold immense promise as cancer biomarkers. However, difficulties in obtaining sufficient quantities of EVs for the identification of potential biomarkers hampers progress in this area. To circumvent this obstacle, we cultured BT-474 breast cancer cells in a two-chambered bioreactor with CDM-HD serum replacement to significantly improve the yield of cancer cell-associated EVs and eliminate bovine EV contamination.

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Trophoblasts are unique epithelial cells found only in the placenta. It has been possible to isolate and maintain human trophoblasts in in vitro culture for many decades. During this period there have been a vast array of media and supplements reported for trophoblast culture and often the reasons for using the media and specific supplements employed in any given laboratory have been lost in the 'mists of time'.

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The release of calcium ions (Ca) from the endoplasmic reticulum (ER) and related store-operated calcium entry (SOCE) regulate maturation of normal megakaryocytes. The -methyl-D-aspartate (NMDA) receptor (NMDAR) provides an additional mechanism for Ca influx in megakaryocytic cells, but its role remains unclear. We created a model of NMDAR hypofunction in Meg-01 cells using CRISPR-Cas9 mediated knockout of the gene, which encodes an obligate, GluN1 subunit of the NMDAR.

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