MOESM3 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 3: Figure S3. α-Mangostin inhibited intracellular FAS activity and reduced the amount of free fatty acids. (A) MDA-MB-231 cells were treated with 0, 1, 2, and 4 μM α-mangostin for 24 h, then intracellular FAS activity was determined spectrophotometrically by measuring the decrease of absorbance at 340 nm due to oxidation of NADPH. (B) MDA-MB-231 cells were treated with 0, 1, 2, and μM α-mangostin for 24 h. Then cells were harvested using trypsin–EDTA, washed twice with PBS. Intracellular fatty acid was determined with a Free Fatty Acid Quantification Kit (Bivision) according to the manufacturer’s instructions. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01

Ordovician chitinozoans of the Miaopo Formation at Zhenjin, Upper Yangtze Platform, South China

Chitinozoan investigations on the late Middle to early Late Ordovician in South China are limited. Documented chitinozoan occurrences are mainly from the Miaopo Formation on the Upper Yangtze Platform. The present study reports new data from the Miaopo Formation at the Zhenjin section in the Yichang area. In total, 13 genera and 33 species are recognised, and three new species are described: Spinachitina? coronifera sp. nov., Lagenochitina yichangella sp. nov. and Pellichitina confragosa sp. nov. The Baltoscandian index species, Laufeldochitina striata, is documented in the lowermost part of the formation. This is the first report of this species in South China. The L. striata Biozone is suggested for the basal part of the formation due to the presence of the eponymous species. The index species of the Laufeldochitina stentor Biozone, the Armoricochitina granulifera and Cyathochitina megacalix subzones adopted in the Jieling section, are also observed in the Zhenjin section. However, according to the new data obtained at Zhenjin, the first appearance datum of C. megacalix and A. granulifera coincides with that of L. striata. Therefore, the C. megacalix Subzone is kept but moved to the L. striata Biozone. Armoricochitina granulifera has stable occurrences in almost the entire Miaopo Formation, corresponding to the Nemagraptus gracilis graptolite biozone. It is slightly older than Baltic records but could be useful for recognising this time interval in South China.</p

sj-jpg-1-imr-10.1177_03000605221108933 - Supplemental material for Lymphocytic myocarditis presenting as acute myocardial infarction: a case report and review of the literature

Supplemental material, sj-jpg-1-imr-10.1177_03000605221108933 for Lymphocytic myocarditis presenting as acute myocardial infarction: a case report and review of the literature by Zhiwei Huang, Guangxun Feng and Yan Liang in Journal of International Medical Research</p

MOESM1 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 1: Figure S1. The effects of α-mangostin on ER stress, autophagy, cell viabilities in MCF-7 cells. (A) MCF-7 cells were treated with 0, 1, 2, and 4 μM α-mangostin for 24 h, and then the relative expression levels of CHOP, BIP, LC3II/LC31 and P62 were analyzed by western blot and were quantified densitometrically with the software ImageJ and calculated according to the reference bands of GAPDH. Data represented the mean ± SD of three independent experiments. **p < 0.01. (B) MCF-7 cells were treated with 4 μm α-mangostin, 5 mM 4PBA, 5 mM 3MA or a combination of them. Cell viabilities were then determined by the CCK-8 assay. Data represented the mean ± SD of three independent experiments. **p < 0.01. (C) MCF-7 cells were treated with/without 4 μm α-mangostin followed 24 h incubation with/without 10 μM PA. Cell viabilities were then determined by the CCK-8 assay. Data represented the mean ± SD of three independent experiments. **p < 0.01

MOESM2 of Alpha-mangostin induces endoplasmic reticulum stress and autophagy which count against fatty acid synthase inhibition mediated apoptosis in human breast cancer cells

Additional file 2: Figure S2. The time-dependent effects of α-mangostin on ER stress and autophagy in MDA-MB-231 cells. Cells were treated with 4 μm α-mangostin for 0, 6, 12, 18, and 24 h, and then the relative expression levels of CHOP, BIP, LC3II/LC31 and P62 were analyzed by western blot and were quantified densitometrically with the software ImageJ and calculated according to the reference bands of GAPDH. Data represented the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01

First-Principles Study of Honeycomb Borophene on the Mo₂C Substrate

Honeycomb borophene (HB) is an important building block for diverse quantum phase observation and applications. However, freestanding HB is energetically unstable, resulting from electron deficiency. Based on a comprehensive first-principles study, we herein predict that the Mo2C monolayer can serve as an effective two-dimensional substrate to prepare planar HB. It is found that the planar HB layer is energetically favorable on the Mo2C substrate with desirable thermal and dynamical stabilities, benefiting from suitable interfacial interactions and electron transfer from Mo2C to HB. In addition, HB is found to be an effective buffer layer to decouple the electronic interactions and modify metal–semiconductor contact. These insightful results not only indicate that the Mo2C substrate is a promising alternative to synthesizing a stable borophene monolayer with pure honeycomb lattice but also provide hints for applications of HB-based materials in high-performance miniaturized electronic devices

Direct Observation of Nucleation and Growth in Amyloid Self-Assembly

Direct Observation of Nucleation and Growth in Amyloid Self-Assembl

Direct Observation of Nucleation and Growth in Amyloid Self-Assembly

Direct Observation of Nucleation and Growth in Amyloid Self-Assembl

Label-Free and Homogenous Detection of Caspase-3-Like Proteases by Disrupting Homodimerization-Directed Bipartite Tetracysteine Display

Caspase-3-like proteases (e.g., caspase-3 and caspase-7) constitute the core players of cell apoptosis, and their dysregulation has been linked to a number of human diseases, such as cancer and neurodegenerative disorders. However, the methods for measuring caspase-3-like proteases are often complex and time-consuming. Herein, we develop a label-free method to homogeneously detect caspase-3-like proteases in vitro and in complex cell lysate. This assay uses a modular peptide that contains a dimerization domain, a caspase-3/7 cleavage sequence, and a dicysteine motif as the activity sensor to detect caspase-3-like proteases. In the absence of caspase-3-like proteases, the homodimerization of modular peptide brings the dicysteine motif into close proximity and forms a particular configuration suitable for the binding to bisarsenical dye FlAsH-EDT2. The coordination of FlAsH-EDT2 to dimeric peptide forms a highly fluorescent FlAsH–peptide complex. In contrast, the cleavage of the modular peptide by caspase-3-like proteases removes the dicysteine motif from the peptide and abrogates the bipartite tetracysteine display, leading to the disappearance of fluorescence. As a result, the caspase-3-like proteases can be quantitatively evaluated by measuring the change in fluorescence. This assay may be carried out in a “mix-and-read” manner and is, thus, quite simple and convenient. Moreover, this assay is extremely specific and can measure caspase-3 protein down to 1.28 × 10–4 μg/mL. Importantly, the assay is compatible with complex biological samples and can measure both the activation and inhibition of intracellular caspase-3, thereby providing a new approach for the screening of caspase-targeted drugs and the diagnosis of apoptosis-associated diseases

Additional file 2 of Identifying patterns of clinical conditions among high-cost older adult health care users using claims data: a latent class approach

Additional file 2: Supplementary Table 1. Selected clinical conditions and related ICD-10 codes