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RISS 인기검색어
- 검색키워드
- 저자 : Yan Meihua (검색결과 4 건)
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Performance of Water-immiscible Silk Fibroin Based Hydrogel as Underwater Biomedical Adhesive
Meihua Yuan,Sheng Yan,Han Liu,S. C. Kundu,Yurong Cai,Juming Yao 한국섬유공학회 2019 Fibers and polymers Vol.20 No.10
The shortcomings of the conventional wound closures like poor wet adhesion strength cause a hydrationpersuadedsoftening, dissolution and viscosity of the adhesives. This happens especially due to the changes in viscosity of theadhesive during underwater surgical operations, which drive the research attention on artificial biomedical adhesives. Theinspiration obtained from the natural protein-based adhesives of marine organisms, we develop a water-immiscible silkprotein fibroin based bioadhesive with the assistance of polyethyleneglycol. The viscosity of the fibroin based bioadhesivecan be modified to meet the application requirement. We adjust the reaction factors like varying the raw materials ratios, pHand gelation time. The fabricated bioadhesive exhibits a high dry adhesive strength of about 120 kPa and an enhanced wetadhesive toughness of about 150 kPa. The adhesive mechanism of the material is also proposed. This simplistic green methodmakes the way for obtaining fibroin based bioadhesive as and when needed. The findings promise the potentiality of the silkfibroin-based biomedical adhesive in future clinical applications.
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Meihua Jin,Yan Wang,Tingting Zhou,Wenzhe Li,Qingping Wen 한국유방암학회 2023 Journal of breast cancer Vol.26 No.3
Purpose: Invasive ductal carcinoma (IDC) accounts for 90% of triple-negative breast cancer (TNBC). IDC is mainly derived from the breast ductal epithelium which is innervated by the 4th to 6th thoracic sympathetic nerves. However, little is known about the contribution of the interactions between sympathetic nerves and breast cancer cells to the malignant progression of TNBC. Methods: The expression levels of the β2-adrenergic receptor (β2-AR, encoded by ADRB2 gene), nerve growth factor (NGF), and tropomyosin receptor kinase A (TrkA) were determined using immunohistochemistry (IHC). NGF expression levels in the serum were compared by enzyme-linked immunosorbent assay (ELISA). Cell proliferation was assessed using the Cell Counting Kit-8 assay. The β2-AR, NGF, p-ERK, and p-CERB expression levels were determined using western blotting. TNBC cells and neuronal cells of the dorsal root ganglion (DRG) in 2-day-old Sprague Dawley rats were co-cultured. Using norepinephrine (NE), NGF, and β2-AR, NGF/TrkA blocker pretreatments, the axon growth of each group of DRG neuron cells was detected by immunofluorescence analysis. Results: The sympathetic adrenergic neurotransmitter NE activated the ERK signaling pathway in TNBC cells. NE/β2-AR signaling promotes NGF secretion. NGF further facilitates the malignant progression of TNBC by increasing sympathetic neurogenesis. In the co-culture assay, the sympathetic adrenergic NE/β2-AR signal pathway also enhanced NGF secretion. NGF binds TrkA in DRG neurons and promotes axonal growth. Conclusion: These results suggest that NE/β2-AR pathway promotes cell proliferation and NGF production in triple-negative breast cancer.
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Jin, Meihua,Jeong, Hae-Kyung,Kim, Tae-Hyung,So, Kang Pyo,Cui, Yan,Yu, Woo Jong,Ra, Eun Ju,Lee, Young Hee Institute of Physics [etc.] 2010 Journal of Physics. D, Applied Physics Vol.43 No.27
<P>We describe the low-temperature thermal exfoliation of graphite oxide to obtain functionalized graphene sheets (FGSs). Graphite oxide, which is highly oxidized graphite produced by a modified Brodie method, is further exfoliated by a simple heat treatment at 270–275 °C under ambient Ar. The FGSs that are generated have fewer defects and less oxygen content than in commercial graphene sheets (GSs) prepared at high temperatures (>900 °C). X-ray photoelectron spectroscopy demonstrates a clear π-plasmon peak in the FGSs of the type that is seen in precursor graphite, but not in commercial GSs. Thus, our FGSs exhibit high 2D crystallinity and minimal defects.</P>
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Li Zhiguo,Shen Hong,Liu Yeqiang,Zhou Xuefeng,Yan Meihua,He Hailan,Zhao Tingting,Zhang Haojun,Li Ping 한국유전학회 2022 Genes & Genomics Vol.44 No.1
Background: Ovarian cancer is a common gynecological malignancy among female patients and poses a serious threat to women's health. Although it has been established that Fos-like antigen 2 (FOSL2) is linked to ovarian cancer (OC), its exact role in the development of OC remains unknown. Objective: This article aims to investigate the role of FOSL2 in ovarian cancer development. Methods: FOSL2 expression in ovarian carcinoma and adjacent tissues was assessed using real-time fluorescent quantitative PCR and western blot. We constructed OE/sh-FOSL2 plasmids and Caspase-1 specific inhibitors (Yvad-CMK) and transfected A 2780 cells with them to identify the relevant cell functions. Furthermore, we used western blot assay to determine the changes in expression of apoptosis-associated speck-like protein containing a CARD (ASC), cysteine aspartate-specific proteasezymogen procaspase 1 (pro-caspase-1), cysteinyl aspartate-specific proteinase-1 (caspase-1), interleukin-1β precursor (pro-IL-1β), interleukin-1β (IL-1β), interleukin-18 precursor (pro-IL-18), and interleukin-18 (IL-18). In addition, we measured the concentration of IL-1β and IL-18 using an enzyme-linked immunosorbent assay (ELISA). Moreover, Tthe level of lactate dehydrogenase (LDH) in the cell supernatant was measured by LDH release assay kit. Results: The expression of FOSL2 was significantly higher compared with the surrounding tissues. The proliferation, migration, and invasion of A2780 cells were enhanced after transfection with OE-FOSL2 plasmids; however, the cell apoptosis was significantly decreased. When FOSL2 was overexpressed, the inflammasome-associated proteins such as ASC, caspase-1, IL-1β, and IL-18 were downregulated. Furthermore, FOSL2 induced apoptosis and activated the production of inflammasomes in A2780 cells. Co-therapy with Yvad-CMK and substantially inhibited apoptosis and activation of inflammasomes. Conclusions: Inhibition of FOSL2 promotes the apoptosis of OC cells by mediating the formation of an inflammasome.
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