Developing
high-performance, flexible, transparent supercapacitors for wearable
electronics represents an important challenge, as it requires active
materials to be sufficiently transparent without compromising energy
storage. Here, we manipulate the morphology of the active materials
and the junctions on the current collector to achieve optimum electronic/ionic
transport kinetics. Two-dimensional Co(OH)2 nanosheets
with single or two layers were vertically aligned onto a modified
Ag nanowires (AgNWs) network using an electrochemical deposition–UV
irradiation approach. The metallic AgNWs network endows high transparency
while minimizing the contact resistance with the pseudocapacitive
Co(OH)2 nanosheets. The Co(OH)2 nanosheets self-assembled
into a three-dimensional array, which is beneficial for the fast ion
movements. The rational materials design greatly boosts the electrochemical
performance of the hybrid network, including an ultrahigh areal capacitance
up to 3108 μC cm–2 (5180 μF cm–2) coupled with long cycle life (20 000 cycles). As a prototype
device, the symmetric supercapacitor well combines high energy/power
density and excellent mechanical flexibility and long-term performance,
suggesting a promising application for the next-generation wearable
electronics.
SummaryDue to differences across species, the mechanisms of cell fate decisions determined in mice cannot be readily extrapolated to humans. In this study, we developed a feeder- and xeno-free culture protocol that efficiently induced human pluripotent stem cells (iPSCs) into PLZF+/GPR125+/CD90+ spermatogonium-like cells (SLCs). These SLCs were enriched with key genes in germ cell development such as MVH, DAZL, GFRα1, NANOS3, and DMRT1. In addition, a small fraction of SLCs went through meiosis in vitro to develop into haploid cells. We further demonstrated that this chemically defined induction protocol faithfully recapitulated the features of compromised germ cell development of PSCs with NANOS3 deficiency or iPSC lines established from patients with non-obstructive azoospermia. Taken together, we established a powerful experimental platform to investigate human germ cell development and pathology related to male infertility.
To satisfy the demand of high power application, lithium-ion batteries (LIBs) with high power density have gained extensive research effort. The pseudocapacitive storage of LIBs is considered to offer high power density through fast faradic surface redox reactions rather than the slow diffusion-controlled intercalation process. In this work, CuCoS anchored on N/S-doped graphene is in situ synthesized and a typical pseudocapacitive storage behavior is demonstrated when applied in the LIB anode. The pseudocapacitive storage and N/S-doped graphene enable the composite to display a capacity of 453 mA h g after 500 cycles at 2 A g and a ultrahigh rate capability of 328 mA h g at 20 A g. We believe that this work could further promote the research on pseudocapacitive storage in transition-metal sulfides for LIBs.
Intrahepatic cholangiocarcinoma (ICC) is a malignant tumor derived from bile duct epithelium. Its characteristics include an insidious onset and frequent recurrence or metastasis after surgery. Current chemotherapies and molecular target therapies provide only modest survival benefits to patients with ICC. Anlotinib is a novel multi-target tyrosine kinase inhibitor that has good antitumor effects in a variety of solid tumors. However, there are few studies of anlotinib-associated mechanisms and use as a treatment in ICC. In this study using in vitro experiments, we found that anlotinib had significant effects on proliferation inhibition, migration and invasion restraint, and cell-cycle arrestment. Anlotinib treatment affected induction of apoptosis and the mesenchymal-epithelial transition. Patient-derived xenograft models generated directly from patients with ICC revealed that anlotinib treatment dramatically hindered in vivo tumor growth. We also examined anlotinib's mechanism of action using transcriptional profiling. We found that anlotinib treatment might mainly inhibit tumor cell proliferation and invasion and promote apoptosis via cell-cycle arrestment by inactivating the VEGF/PI3K/AKT signaling pathway, as evidenced by significantly decreased phosphorylation levels of these kinases. The activation of vascular endothelial growth factor receptor 2 (VEGFR2) can subsequently activate PI3K/AKT signaling. We identified VEGRF2 as the main target of anlotinib. High VEGFR2 expression might serve as a promising indicator when used to predict a favorable therapeutic response. Taken together, these results indicated that anlotinib had excellent antitumor activity in ICC, mainly via inhibiting the phosphorylation level of VEGFR2 and subsequent inactivation of PIK3/AKT signaling. This work provides evidence and a rationale for using anlotinib to treat patients with ICC in the future.
Highlights • CD13 expression is higher in more metastatic HCC samples and its overexpression predicts worse prognosis in HCC patients. • CD13 regulates HCC cell proliferation, invasion, primary tumor growth and sorafenib resistance. • CD13-HDAC5-LSD1-NF-#x003BA;B signaling axis is a newly identified signaling axis in HCC. • CD13 inhibitor Ubenimex restored sorafenib sensitivity in HCC.
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