Why do supply chain technologies sometimes fail to improve a firm’s performance?

Successful implementation depends on the reason why the technology was adopted in the first place, write Zhongzhi Liu, Daniel Prajogo, and Adegoke Ok

Additional file 1: of Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma

Figure S1. The cell numbers of RU cells derived from SupM2 and Karpas 299 upon various doses of H2O2 treatment were counted by trypan blue exclusion assay from day 0 to day 3. (PDF 79 kb

Additional file 2: of Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma

Figure S2. Anti-oxidant reagent NAC blocked the increase of GFP-positive cells induced by H2O2. A-B) Treatment of NAC abrogated the increased GFP-positive cells induced by 0.3 mM H2O2 for 48 h in RU cells derived from SupM2 in a NAC-dose dependent manner, read by GFP expression (A) and luciferase activity (B). (PDF 55 kb

Additional file 5: of Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma

Figure S5. The activation levels of ALK and STAT3 were inappreciably changed upon H2O2 re-challenge. The expression levels of pALKY1604, ALK, pSTAT3Y705, and STAT3 in RU and RR cells with or without H2O2 re-challenge. The same cell lysates from Fig. 3a were reused in this experiment, and note that the same β-actin blot as the one in Fig. 3a was recycled for H2O2-stimulation in RU and RR cells derived from Karpas 299 cells. (PDF 102 kb

Additional file 6: of Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma

Figure S6. RU cells derived from SupM2 were transfected with either Sox2 siRNA or scrambled siRNA which served as a negative control. Cells after siRNA transfection were exposed to 0.3 mM H2O2 re-challenge. At day 4 of the H2O2 re-challenge experiment; cells were subjected to 200 ng/mL doxorubicin for additional 48 h, following by the trypan blue exclusion assay-based cell viability analysis. The Western blots in the right panel demonstrated the Sox2 knockdown efficiency in RU cells from SupM2 24 h post transfection. (PDF 48 kb

MOESM1 of Endoplasmic reticulum stress in perivascular adipose tissue promotes destabilization of atherosclerotic plaque by regulating GM-CSF paracrine

Additional file 1. PVAT promotes destabilization of atherosclerotic plaque

Acidity Considerations in the Self-Assembly of POM/Ag/trz-Based Compounds with Efficient Electrochemical Activities in LIBs

Controlled self-assembly of the inorganic–organic hybrid compounds based on polyoxometalates (POMs) is hampered by the wide range of oxo and hydroxo units on the peripheries of POMs and many chemical parameters. In this work, aiming to understand the pH value influence on the POM/Ag/trz assembly (trz = 1,2,3-triazole), two new hybrid compounds based on POMs combining with metal–organic frameworks (MOFs), H­[Ag₂₇(trz)₁₆(H₂O)₄]­[(AsW₁₂O₄₀)₂] (<b>1</b>), and [Ag₁₅(trz)₈]­[AsW₁₂O₄₀] (<b>2</b>), were isolated under different pH value. The structural analysis reveals that the [Ag₇(trz)₄]³⁺ subunits and Keggin-type arsenotungstate are assembled into a complicated three-dimensional framework containing two distinct types of channels in compound <b>1</b>. And the [Ag₅(trz)₄]⁺ subunits and Keggin-type arsenotungstate are assembled into a three-dimensional framework containing the single channel under the aid of Ag–Ag bonds in compound <b>2</b>. In addition, compounds <b>1</b> and <b>2</b> were employed as anode materials of lithium-ion batteries (LIBs) and exhibited the promising electrochemical performances

Additional file 1 of Serum CTRP9 and high-molecular weight adiponectin are associated with ischemic stroke

Additional file 1: Table S1. Serum concentration of CTRP9 and APN in patients of different infarct stages

Table_1_RETRACTED: Mitochondrial Fission and Mitophagy Reciprocally Orchestrate Cardiac Fibroblasts Activation.docx

Although mitochondrial fission has been reported to increase proliferative capacity and collagen production, it can also contribute to mitochondrial impairment, which is detrimental to cell survival. The aim of the present study was to investigate the role of mitochondrial fission in cardiac fibroblasts (CF) activation and explore the mechanisms involved in the maintenance of mitochondrial health under this condition. For this, changes in the levels of mitochondrial fission/fusion-related proteins were assessed in transforming growth factor beta 1 (TGF-β1)-activated CF, whereas the role of mitochondrial fission during this process was also elucidated, as were the underlying mechanisms. The interaction between mitochondrial fission and mitophagy, the main defense mechanism against mitochondrial impairment, was also explored. The results showed that the mitochondria in TGF-β1-treated CF were noticeably more fragmented than those of controls. The expression of several mitochondrial fission-related proteins was markedly upregulated, and the levels of fusion-related proteins were also altered, but to a lesser extent. Inhibiting mitochondrial fission resulted in a marked attenuation of TGF-β1-induced CF activation. The TGF-β1-induced increase in glycolysis was greatly suppressed in the presence of a mitochondrial inhibitor, whereas a glycolysis-specific antagonist exerted little additional antifibrotic effects. TGF-β1 treatment increased cellular levels of reactive oxygen species (ROS) and triggered mitophagy, but this effect was reversed following the application of ROS scavengers. For the signals mediating mitophagy, the expression of Pink1, but not Bnip3l/Nix or Fundc1, exhibited the most significant changes, which could be counteracted by treatment with a mitochondrial fission inhibitor. Pink1 knockdown suppressed CF activation and mitochondrial fission, which was accompanied by increased CF apoptosis. In conclusion, mitochondrial fission resulted in increased glycolysis and played a crucial role in CF activation. Moreover, mitochondrial fission promoted reactive oxygen species (ROS) production, leading to mitophagy and the consequent degradation of the impaired mitochondria, thus promoting CF survival and maintaining their activation.</p