Design of iron oxyhydroxide nanosheets coated on Co species embedded in nanoporous carbon for oxygen evolution reaction.

There is still a tremendous challenge in designing environmentally friendly oxygen evolution reaction (OER) catalysts that are inexpensive and high-performing for practical applications. Herein, the self-sacrificing template zeolitic imidazolate framework-67 (ZIF-67) was pyrolyzed under N2 atmosphere to generate Co species embedded in nanoporous carbon (Co-NC). Then, iron oxyhydroxide (FeOOH) was wrapped onto the Co-NC surface via electrodeposition to shape the Co-NC@FeOOH composites. Benefiting from the core-shell structure, high conductivity, and distributed active sites, Co-NC@FeOOH presents distinguished OER performance with a low overpotential (336 mV) at 10 mA cm-2 and small Tafel slope (49.46 mV dec-1). This work furnishes a rosy passage for receiving cost-effective electrocatalysts with high efficiency for OER.

Facile synthesis of Co-Ni layered double hydroxides nanosheets wrapped on a prism-like metal-organic framework for efficient oxygen evolution reaction.

The construction of low-cost oxygen evolution reaction (OER) electrocatalysts with high activity and good durability is a considerable challenge for facilitating the efficient utilization of green energy. Herein, the prism-like materials of institute lavoisier frameworks-88 (MIL-88) was first synthesized by a hydrothermal method. Then, Co-Ni layered double hydroxides (CoNi-LDHs) nanosheets were directly wrapped on the MIL-88 surface by electrodeposition to form core-shell MIL-88@CoNi-LDHs composites. Due to the distinct structure and synergistic effect between the MIL-88 core and CoNi-LDHs shell, it was found that MIL-88@CoNi-LDHs had outstanding OER activity with a small Tafel slope (45.55 mV dec-1), low overpotential (314 mV) at 10 mA cm-2, and superior durability. This study provides a prospective pathway to exploit highly efficient low-cost electrocatalysts for OER.

Ovarian cancer treatment and natural killer cell-based immunotherapy.

Background: Ovarian cancer (OC) is one of the malignant tumors that poses a serious threat to women's health. Natural killer (NK) cells are an integral part of the immune system and have the ability to kill tumor cells directly or participate indirectly in the anti-tumor immune response. In recent years, NK cell-based immunotherapy for OC has shown remarkable potential. However, its mechanisms and effects remain unclear when compared to standard treatment. Methods: To explore the value of NK cell-based immunotherapy in the treatment of OC, we conducted a literature review. In comparison to standard treatment, our focus was primarily on the current anti-tumor mechanisms, the clinical effect of NK cells against OC, factors affecting the structure and function of NK cells, and strategies to enhance the effectiveness of NK cells. Results: We found that NK cells exert their therapeutic effects in OC through mechanisms such as antibody-dependent cell cytotoxicity, perforin release, and granule enzyme secretion. They also secrete IFN-γ and TNF-α or engage in Fas/FasL and TRAIL/TRAILR pathways, mediating the death of OC cells. In clinical trials, the majority of patients experienced disease stability with mild side effects after receiving NK cell-based immunotherapy, but there is still a lack of high-quality research evidence regarding its clinical effectiveness. OC and prior experience with standard treatments have an effect on NK cells, and it may be considered to maximize NK cell effects through the modulation of the tumor microenvironment or combination with other therapies. Conclusions: In this review, we have summarized the current evidence of NK cell applications in the treatment of OC. Furthermore, factors and strategies that influence and enhance the role of NK cell immunotherapy are discussed.

miR-146a-5p Plays an Oncogenic Role in NSCLC via Suppression of TRAF6.

Non-small cell lung cancer (NSCLC) is the most deadly cancer in the world due to its often delayed diagnosis. Identification of biomarkers with high sensitivity, specificity, and accessibility for early detection, such as circulating microRNAs, is therefore of utmost importance. In the present study, we identified a significantly higher expression of miR-146a-5p in the serum and tissue samples of NSCLC patients than that of the healthy controls. In parallel, miR-146a-5p was also highly expressed in three human NSCLC adenocarcinoma-cell lines (A549, H1299, and H1975) compared to the human bronchial epithelium cell line (HBE). By dual-luciferase reporter assay and manipulation of the expressions of miR-146a-5p and its target gene, tumor necrosis factor receptor-associated factor 6 (TRAF6), we showed that the functional effects of miR-146a-5p on NSCLC cell survival and migration were mediated by direct binding to and suppression of TRAF6. Overexpression of TRAF6 sufficiently reversed miR-146a-5p-induced cancer cell proliferation, migration, and apoptosis resistance. Our data implied that miR-146a-5p/TRAF6/NF-κB-p65 axis could be a promising diagnostic marker and a therapeutic target for NSCLC.

APS could potentially activate hepatic insulin signaling in HFD-induced IR mice.

Astragalus polysaccharide (APS) is the main component of Astragalus membranaceus, an anti-diabetic herb being used for thousands of years in Traditional Chinese medicine (TCM). In this study, we aimed to evaluate the impact of APS on hepatic insulin signaling, autophagy and ER stress response in high-fat-diet (HFD)-induced insulin resistance (IR) mice. APS was intra-gastrically administrated and metformin was used as a control medicine. Apart from monitoring the changes in the important parameters of IR progression, the gene and protein expression of the key factors marking the state of hepatic ER stress and autophagic flux were examined. We found that, largely comparable to the metformin regime, APS treatment resulted in an overall improvement of IR, as indicated by better control of body weight and blood glucose/lipid levels, recovery of liver functions and regained insulin sensitivity. In particular, the excessive and pro-apoptotic ER stress response and inhibition of autophagy, as a result of prolonged HFD exposure, were significantly corrected by APS administration, indicating a switch of the cellular fate in favor of cell survival. Using the HepG2/IR cell model, we demonstrated that APS modulated the insulin-initiated phosphorylation cascades in a similar manner to metformin. This study provides a rationale for exploiting the insulin-sensitizing potential of APS, which has a therapeutic performance almost equivalent to metformin, to enrich our options in the treatment of IR.