Induced pluripotent stem cells (iPSCs) have differentiation potential into different somatic cell types in vitro and are a useful tool to investigate pathomechanistic and cellular processes. In this study, we generated human induced pluripotent stem cells (iPSC) ZZUNEUi012-A from an apparently healthy female individual using an integration-free reprogramming method. The generated hiPSC line was pluripotent and had normal karyotype, showed robust expression of pluripotency markers and could differentiate into all three germ layers in vitro.Induced pluripotent stem cell (iPSC) line HUi002-A was reprogrammed from skin fibroblasts via non-integrating, virus free self-replicating RNA. Skin fibroblasts from a 53-year-old male Caucasian, non-familial Parkinson's disease patient, idiopathic (clinical summary confirmed Parkinson's disease) was obtained from the Coriell Institute (AG20442). Generated iPSCs were characterized and pluripotency was confirmed.COX6A2 protein is a structural subunit of Complex IV (CIV/Cytochrome c oxidase/COX) in the mitochondrial respiratory chain. It is mainly expressed in the heart and skeletal muscle, also in some interneurons, regulating the assembly and catalytic activity of CIV. Its mutations can lead to COX deficiency, causing human myopathies, and maybe a potential cause of neurological abnormalities. Here, we used the CRISPR/Cas9 editing system to establish a homozygous COX6A2 knockout (COX6A2-KO) human embryonic stem cell (hESC) line. https://www.selleckchem.com/products/cid44216842.html This COX6A2-KO hESC has normal morphology, pluripotency, and karyotype, which can differentiate into three germ layers in vivo.Pancreatic cancer has the worst prognosis of all cancers due to disease aggressiveness and paucity of early detection platforms. We developed biomaterial scaffolds that recruit metastatic tumor cells and reflect the immune dysregulation of native metastatic sites. While this platform has shown promise in orthotopic breast cancer models, its potential in other models is untested. Herein, we demonstrate that scaffolds recruit disseminated pancreatic cells in the KPCY model of spontaneous pancreatic cancer prior to adenocarcinoma formation (3-fold increase in scaffold YFP + cells). Furthermore, immune cells at the scaffolds differentiate early- and late-stage disease with greater accuracy (0.83) than the natural metastatic site (liver, 0.50). Early disease was identified by an approximately 2-fold increase in monocytes. Late-stage disease was marked by a 1.5-2-fold increase in T cells and natural killer cells. The differential immune response indicated that the scaffolds could distinguish spontaneous pancreatic cancer from spontaneous breast cancer. Collectively, our findings demonstrate the utility of scaffolds to reflect immunomodulation in two spontaneous models of tumorigenesis, and their particular utility for identifying early disease stages in the aggressive KPCY pancreatic cancer model. Such scaffolds may serve as a platform for early detection of pancreatic cancer to improve treatment and prognosis.Antithrombogenicity, anti-inflammation, and rapid re-endothelialization are central requirements for the long-term success of cardiovascular stents. In this work, a plant-inspired phenolic-amine chemistry strategy was developed to combine the biological functions of a plant polyphenol, tannic acid (TA), and the thrombin inhibitor bivalirudin (BVLD) for tailoring the desired multiple surface functionalities of cardiovascular stents. To realize the synergistic modification of TA and BVLD on a stent surface, an amine-bearing coating of plasma polymerized allylamine was firstly prepared on the stent surface, followed by the sequential conjugation of TA and BVLD in alkaline solution based on phenolic-amine chemistry (i.e., Michael addition reaction). TA and BVLD were successfully immobilized onto the stent surface with considerable amounts of 330 ± 12 and 930 ± 80 ng/cm2, respectively. The abundant phenolic hydroxyl groups of TA imparted the stent with ability to suppress inflammation. Meanwhile, BVLD provided an antithrombogenic and endothelial-friendly microenvironment. As a result, the combined functions of the TA and BVLD facilitate the rapid stent re-endothelialization for reduced intimal hyperplasia in vivo, and may be a promising strategy to address the clinical complications associated with restenosis and late stent thrombosis.Several bird species have adapted to foraging in landfills, although these sites are known to represent significant sources of emissions of toxic semi-volatile chemicals including the halogenated flame retardants (HFRs) (e.g., polybrominated diphenyl ethers (PBDEs) and emerging compounds). The objective of this study was to investigate the association between atmospheric exposure to PBDEs and selected emerging HFRs and their bioaccumulation in landfill-foraging birds. We determined HFR concentrations in liver of 58 GPS-tagged ring-billed gulls (Larus delawarensis) breeding in a colony near Montreal (Canada) as well as their atmospheric exposure determined using a miniature bird-borne passive air sampler. PBDE mixtures were the most abundant HFRs determined in passive air samplers (daily exposure rates of ∑9PentaBDE 47.4 ± 6.5 pg/day; DecaBDE 36.0 ± 6.3 pg/day, and ∑3OctaBDE 3.4 ± 0.5 pg/day) and liver (∑9PentaBDE 68.1 ± 8.9 ng/g ww; DecaBDE 52.3 ± 8.1 ng/g ww, and ∑3OctaBDE 12.8 ± 2.1 ng/g ww), and their concentrations increased with the presence probability of gulls in landfills. We found a spatial relationship between the local sources of atmospheric exposure to PBDEs and the sites associated with greatest PBDE concentrations in liver. Specifically, the atmospheric exposure index was correlated with the bioaccumulation index (Pearson r for ∑9PentaBDE r = 0.63, p less then 0.001; DecaBDE r = 0.66, p less then 0.001, and ∑3OctaBDE r = 0.42, p less then 0.001). However, we found no correlation at the individual level between daily exposure rates of HFRs in passive air samplers and their liver concentrations. This suggests that complex exposure pathways combined with toxicokinetic factors shaped HFR profiles in gull liver, potentially confounding the relationships with atmospheric exposure.