15 research outputs found
Electrospun Nanofibers Modified with Copper Nanoparticles for Simultaneous Extraction and Detection of Three Ochratoxins in Foods
In this study, several electrospun nanofibers were prepared
and
characterized, and the electrospun polystyrene/poly(ether sulfone)
nanofiber coated with copper nanoparticles (PS/PES-CuNP nanofibers)
was selected and utilized as solid-phase extraction adsorbent. And
then, the packed-fiber solid-phase extraction coupled with high-performance
liquid chromatography-fluorescence detection method was established
for the efficient determination of ochratoxins in foods. With the
proposed method, several factors including the type and dosage of
nanofibers, sample pH, extraction time, type, and volume of elution
solvent were optimized. The results suggested that low limit of detection
(0.102–0.126 ng/mL), limit of quantification (0.382–0.436
ng/mL), and recoveries (85.5–111.1%) for ochratoxin A, B, and
C with relative standard deviations <7% were achieved. As-synthesized
PS/PES-CuNP nanofibers displayed satisfactory potential practical
application in the simultaneous pretreatment and determination of
mycotoxins in complex matrice samples
Table4_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.XLSX
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
Table3_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.XLSX
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
Table2_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.XLSX
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
Image1_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.PNG
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
DataSheet1_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.docx
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
Table1_EZH2-mediated H3K27me3 is a predictive biomarker and therapeutic target in uveal melanoma.XLSX
Although gene mutations and aberrant chromosomes are associated with the pathogenesis and prognosis of uveal melanoma (UM), potential therapeutic targets still need to be explored. We aim to determine the predictive value and potential therapeutic target of EZH2 in uveal melanoma. Eighty-five uveal melanoma samples were recruited in our study, including 19 metastatic and 66 nonmetastatic samples. qRT-PCR, immunohistochemistry staining, and western blotting were applied to detect the expression of EZH2 and H3K27me3. We found that EZH2 (41/85, 48.24%) and H3K27me3 (49/85, 57.65%) were overexpressed in uveal melanoma. The expression of EZH2 was not significantly associated with metastasis. High H3K27me3 expression was correlated with poor patient prognosis. UNC 1999, an EZH2 inhibitor, can downregulate H3K27me3 expression and has the most potency to inhibit OMM1 cell growth by the cell cycle and ferroptosis pathway. These results indicate that H3K27me3 can be a biomarker predicting a poor prognosis of UM. EZH2 is the potential therapeutic target for UM.</p
Protein-Directed Synthesis of Bifunctional Adsorbent-Catalytic Hemin-Graphene Nanosheets for Highly Efficient Removal of Dye Pollutants via Synergistic Adsorption and Degradation
Herein,
for the first time, we report a “green”,
one-pot reduction/decoration method for the synthesis of bifunctional
adsorbent-catalytic hemin-graphene nanosheets by using a common available
protein (bovine serum albumin, BSA) as both a reductant and a stabilizer.
Our prepared nanosheets are highly stable and possess intrinsic peroxidase-like
catalytic activity due to the decoration of BSA and hemin. Furthermore,
benefiting from the combined advantages of graphene and BSA, these
nanosheets are able to efficiently adsorb dye pollutants from aqueous
solution. More importantly, due to their adsorption and catalytic
ability, these adsorbent-catalytic nanosheets can be applied to highly
efficient dye removal via synergistic adsorption and degradation.
Specifically, our catalysts can easily bring organic dyes to their
surface by adsorption, and then activate H<sub>2</sub>O<sub>2</sub> to generate hydroxyl radicals, leading to the degradation of the
dyes. Such catalytic mechanism of our as-prepared nanosheets was analogous
to that of natural enzymes, in which the extremely high catalytic
efficiency is largely dependent upon their ability to bring substrates
in close proximity to the active sites of enzymes. Our finding may
open new potential applications of hemin-graphene hybrid nanosheets
in environmental chemistry, biotechnology, and medicine
SIRT3 Enhances Glycolysis and Proliferation in SIRT3-Expressing Gastric Cancer Cells
<div><p>SIRT3 is a key NAD<sup>+</sup>-dependent protein deacetylase in the mitochondria of mammalian cells, functioning to prevent cell aging and transformation via regulation of mitochondrial metabolic homeostasis. However, SIRT3 is also found to express in some human tumors; its role in these SIRT3-expressing tumor cells needs to be elucidated. This study demonstrated that the expression of SIRT3 was elevated in a group of gastric cancer cells compared to normal gastric epithelial cells. Although SIRT3 expression levels were increased in the gastric tumor tissues compared to the adjacent non-tumor tissues, SIRT3 positive cancer cells were more frequently detected in the intestinal type gastric cancers than the diffuse type gastric cancers, indicating that SIRT3 is linked with subtypes of gastric cancer. Overexpression of SIRT3 promoted cell proliferation and enhanced ATP generation, glucose uptake, glycogen formation, MnSOD activity and lactate production, which were inhibited by SIRT3 knockdown, indicating that SIRT3 plays a role in reprogramming the bioenergetics in gastric tumor cells. Further analysis revealed that SIRT3 interacted with and deacetylated the lactate dehydrogenase A (LDHA), a key protein in regulating anaerobic glycolysis, enhancing LDHA activity. In consistence, a cluster of glycolysis-associated genes was upregulated in the SIRT3-overexpressing gastric tumor cells. Thus, in addition to the well-documented SIRT3-mediated mitochondrial homeostasis in normal cells, SIRT3 may enhance glycolysis and cell proliferation in SIRT3-expressing cancer cells.</p></div
Overexpression of SIRT3 enhances glycolysis in gastric cancer cells.
<p>Glucose uptake, lactate production and glycogen formation were measured in AGS (A, C, E) and SGC-7901 (B, D, F) cells with SIRT3 overexpression or knockdown. All data are presented as mean ± S.E. (n = 3; *, <i>p</i> < 0.05; **, <i>p</i> < 0.01).</p