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Pixel Grafting: The sunday paper Skin Graft Expansion Method.
Acute kidney injury (AKI) is a severe complication of autologous orthotopic liver transplantation (AOLT). Apoptosis has been shown to be involved in renal ischemia/reperfusion, and the PI3K/AKT signaling pathway is involved in numerous cell processes, including promoting cell survival and inhibiting apoptosis. We aimed to verify whether the PI3K/AKT signaling pathway participates in the development of post-AOLT AKI.

Male Sprague-Dawley rats underwent AOLT with or without treatment with insulin-like growth factor-1 (IGF-1, a PI3K/AKT activator) and LY294002 (a PI3K/AKT inhibitor; n=8/group). NRK-52E cells (rat renal tubular epithelial cell line) were subjected to hypoxia-re-oxygenation to mimic renal cell I/R injury in vitro, and confirm whether silencing information regulator 1 (SIRT1) mediated the protective effects of PI3K/AKT by deacetylating forkhead protein O3a (FoxO3a).

During the reperfusion stage, kidney injury peaked at 8h after reperfusion, then gradually recovered, which was consistent with the dynamic changes in apoptosis and the protein expressions of Bcl-2 interacting mediator of cell death (Bim), Fas ligand (FasL), and nuclear FoxO3a AKT phosphorylation and nuclear SIRT1 protein expression were also upregulated. IGF-1 application decreased Bim, FasL, and nuclear FoxO3a protein expressions, and protected against apoptosis and AKI. In NRK-52E cells, IGF-1 upregulated nuclear SIRT1 expression, reduced FoxO3a acetylation, downregulated Bim and FasL protein expressions, and attenuated apoptosis and AKI; these effects were reversed by SIRT1 blocking.

The activation of the PI3K/AKT signaling pathway not only induced FoxO3a nuclear export but also deacetylation through upregulating nuclear SIRT1 expression to attenuate post-AOLT AKI.
The activation of the PI3K/AKT signaling pathway not only induced FoxO3a nuclear export but also deacetylation through upregulating nuclear SIRT1 expression to attenuate post-AOLT AKI.
To investigate the biomimetic fabrication of fibrous-like organic-inorganic hybrid structures via a simple bottom-up approach, viz. self-assembly of simple molecules, and apply fibrous-like composites as a novel primer to improve dentin bond strengths of self-etch adhesives.

The resultants of commercial amorphous calcium phosphate (ACP) nanoparticles and 10-methacryloyloxydecyl dihydrogen phosphate (MDP) ethanol-aqueous solution were analyzed by TEM, SEM, XRD, DLS and AFM. The acid and alkali resistance of abovementioned self-assembled composites were analyzed with TEM. Micro-tensile bond strengths (MTBS) tests were performed after polished dentin surfaces were pretreated with self-assembled composites. The pretreated dentin surfaces and dentin-resin interfaces were characterized by SEM/TEM.

ACP nanoparticles in MDP solution could self-assemble into fibrous-like nanotube structures in 8nm diameter. Self-assembly and self-proliferation process went from ACP nanoparticles, dissolved ACP nanoparticles (leslf-etch adhesives greatly improved dentin bond strengths.The adrenal glands have striking morpho-biochemical features that render them vulnerable to the effects of toxins.
This study was conducted to explore the therapeutic utility of extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSC-EVs) against fluoride-induced adrenal toxicity.

The work included isolation and further identification of BMSC-EVs by transmission electron microscopy and flow cytometric analysis. Adrenal toxicity in rats was induced by oral administration of 300ppm of sodium fluoride (NaF) in drinking water for 60days followed by a single dose injection of BMSC-EVs. The effects of BMSC-EVs against NaF was evaluated by adrenal oxidant/antioxidant biomarkers, hormonal assay of plasma adrenocorticotrophic hormone (ACTH) and corticosterone (CORT) and mRNA gene expression quantitation for adrenal cortical steroidogenic pathway-encoding genes. Histopathological examination of the adrenal tissue was performed.

BMSC-EVs were effectively isolated and characterized. NaF exposure decreased adrenal superoxide dismutase and catalase activities, increased adrenal malondialdehyde levels, elevated plasma ACTH, diminished CORT concentrations and downregulated the adrenal cortical steroidogenic pathway-encoding genes. In addition, NaF-induced marked adrenal histopathological lesions.

BMSC-EVs treatment repaired damaged adrenal tissue and recovered its function greatly following NaF consumption. BMSC-EVs reversed the toxic effects of NaF and reprogramed injured adrenal cells by activating regenerative processes.
BMSC-EVs treatment repaired damaged adrenal tissue and recovered its function greatly following NaF consumption. BMSC-EVs reversed the toxic effects of NaF and reprogramed injured adrenal cells by activating regenerative processes.Biosensors are important devices in clinical diagnostics, food processing, and environmental monitoring for detecting various analytes, especially viruses. These biosensors provide rapid and effective instruments for qualitative and quantitative detection of infectious diseases in real-time. Here, we report the development of biosensors based on various techniques. Additionally, we will explain the mechanisms, advantages, and disadvantages of the most common biosensors that are currently used for viral detection, which could be optical (e.g., surface-enhanced Raman scattering (SERS), Surface plasmon resonance (SPR)) and electrochemical biosensors. Based on that, this review recommends methods for efficient, simple, low-cost, and rapid detection of SARS-CoV-2 (the causative agent of COVID-19) that employ the two types of biosensors depending on attaching hemoglobin β-chain and binding of specific antibodies with SARS-CoV-2 antigens, respectively.
We evaluated the effect of H3K9ac modification on the transcriptional level of Pik3ca and the apoptosis induction effects of Pik3ca in the PI3K/AKT pathway in rat H9C2 cells.

H9C2 cells were cultured with 1uM doxorubicin for 8 h. The acetylation level of histone H3K9 in the transcriptional initiation area of Pik3ca was determined by CHIP-seq. The enrichment of mRNA fragment of Pik3ca transcription initiation region by H3K9ac antibody was detected by CHIP-qPCR, and the expression of Pik3ca was detected by real-time Polymerase Chain Reaction(rt-PCR) and western blot. The transcription efficiency of Pik3ca siRNA was detected by immunofluorescence and western blot. Cell Counting Kit8(CCK8) was used to detect the cell activity and flow cytometry was used to detect the apoptosis rate. TLR2-IN-C29 Western blot was applied to assess the protein expression level of PI3K, P-AKT, AKT, Bcl2, BAX and cleaved-caspase3 in H9C2 cells.

In doxorubicin-inducedH9C2 cells, the acetylation levels of histone H3K9 in the Pik3ca transcriptional initiation region significantly increased and promoted the transcription of Pik3ca.
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