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Carboxymethyl pachymaran （CMP） is a carboxymethylated modification product of the water-insoluble polysaccharides from Poria cocos. It has many biological activities such as immune regulation, antibacterial, anti-inflammatory, anti-tumor, anti-oxidation, liver damage protection and intestinal flora regulation. It has a wide application prospect in functional food, active molecular carrier, medicine and other fields. In this paper, the research of CMP at home and abroad in recent years was focused, the biological activity, preparation, identification and application development of CMP were reviewed, and the future development direction of CMP was prospected.

Background: Chronic kidney disease (CKD) is a leading cause of death in the United States, and renal fibrosis represents a pathologic hallmark of CKD. Extracellular cold-inducible RNA-binding protein (eCIRP) is a stress response protein involved in acute inflammation, tissue injury and regulated cell death. However, the role of eCIRP in chronic inflammation and tissue injury has not been elucidated. We hypothesize that eCIRP is involved in renal ischemia/reperfusion (RIR)-induced CKD and that C23, an antagonist to eCIRP, is beneficial in attenuating renal fibrosis and ferroptosis in RIR-induced CKD. Methods: C57BL/6 (WT) or CIRP−/− mice underwent renal injury with total blockage of blood perfusion by clamping bilateral renal pedicles for 28 min. In the WT mice at the time of reperfusion, they were treated with C23 (8 mg/kg) or vehicle. Blood and kidneys were harvested for further analysis at 21 days thereafter. In a separate cohort, mice underwent bilateral RIR and treatment with C23 or vehicle and were then subjected to left nephrectomy 72 h thereafter. Mice were then monitored for additional 19 days, and glomerular filtration rate (GFR) was assessed using a noninvasive transcutaneous method. Results: In the RIR-induced CKD, CIRP−/− mice showed decreased collagen deposition, fibronectin staining, and renal injury as compared to the WT mice. Administration of C23 ameliorated renal fibrosis by decreasing the expression of active TGF-β1, α-SMA, collagen deposition, fibronectin and macrophage infiltration to the kidneys. Furthermore, intervention with C23 significantly decreased renal ferroptosis by reducing iron accumulation, increasing the expression of glutathione peroxidase 4 (GPX4) and lipid peroxidation in the kidneys of RIR-induced CKD mice. Treatment with C23 also attenuated BUN and creatinine. Finally, GFR was significantly decreased in RIR mice with left nephrectomy and C23 treatment partially prevented their decrease. Conclusion: Our data show that eCIRP plays an important role in RIR-induced CKD. Treatment with C23 decreased renal inflammation, alleviated chronic renal injury and fibrosis, and inhibited ferroptosis in the RIR-induced CKD mice. [ABSTRACT FROM AUTHOR]

Necroptosis is a type of regulated cell death (RCD) that is triggered by changes in the extracellular or intracellular milieu that are picked up by certain death receptors. Thanks to its potent capacity to induce immunological responses and overcome apoptotic resistance, it has garnered significant attention as a potential cancer treatment. Basic information for the creation of nano-biomedical treatments is provided by studies on the mechanisms underlying tumor necroptosis. Receptor-interacting protein kinase 1 (RIPK1)–RIPK3-mediated necroptosis, Toll-like receptor domain-containing adapter-inducing interferon (IFN)-β (TRIF)–RIPK3-mediated necroptosis, Z-DNA-binding protein 1 (ZBP1)–RIPK3-mediated necroptosis, and IFNR-mediated necroptosis are the four signaling pathways that collectively account for triggered necroptosis in this review. Necroptosis has garnered significant interest as a possible cancer treatment strategy because, in contrast to apoptosis, it elicits immunological responses that are relevant to therapy. Thus, a thorough discussion is held on the connections between tumor cell necroptosis and the immune environment, cancer immunosurveillance, and cells such as dendritic cells (DCs), cytotoxic T cells, natural killer (NK) cells, natural killer T (NKT) cells, and their respective cytokines. Lastly, a summary of the most recent nanomedicines that cause necroptosis in order to cause immunogenic cell death is provided in order to emphasize their promise for cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Alkaline water electrolysis is a commercially viable technology for green H2 production using renewable electricity from intermittent solar or wind energy, but very few non‐noble bifunctional catalysts simultaneously exhibit superb catalytic efficiency and stability at large current densities for hydrogen and oxygen evolution reactions (HER and OER, respectively), especially for iron‐based catalysts. Given that iron is the most abundant and least expensive transition metal, iron‐based compounds are very attractive low‐cost targets as active electrocatalysts for bifunctional water splitting with large‐current durability. Herein, the in situ construction of a self‐supported Fe2P/Co2N porous heterostructure arrays possessing superb bifunctional catalytic activity in base is reported, featured by low overpotentials of 131 and 283 mV to attain a current density of 500 mA cm−2 for HER and OER, respectively, outperforming most of non‐noble bifunctional electrocatalysts reported hitherto. Particularly, this hybrid catalyst also displays an excellent overall water splitting activity, requiring low voltages of 1.561 and 1.663 V to attain 100 and 500 mA cm−2 with excellent durability in 1 m KOH, respectively. Most importantly, the catalyst is stable for >120 h, even when the current density is 500 mA cm−2, which is prominently superior to IrO2(+)//Pt(−) coupled noble electrodes, and is among the very best bifunctional catalysts reported thus far. Detailed theoretical calculations reveal that the interfacial interaction between Fe2P and Co2N can further improve the H* binding energy at the iron sites. [ABSTRACT FROM AUTHOR]

This paper consists of two parts: aerodynamic and mechanical multi-objective optimization for centrifugal compressor impeller through combining the three dimensional fluid dynamic simulation module CFX 16.1, the static structure in the ANSYS Workbench and the optimization software optiSLang; and a comparison and analysis of the effects of the optimized compressor on the engine performance by the one dimensional simulation tool GT-Power. In the process of optimization, the compressor design point is regarded as the optimizing point, while impeller blades and hub line were parameterized through the Bezier curve. Pressure ratio, isentropic efficiency, quality and maximum deformation and maximum internal stress of the impeller were defined as the output conditions. MOP module was then adopted in optiSLang for the parameters sensitivity analysis and mapping relationship modeling between the impeller parameters and the objective functions. The genetic algorithm is applied to find out and validate the optimal design. Through 1D simulation tool GT-Power, the influence of the optimized compressor on rotational speed of the turbocharger, backpressure and pumping loss under different engine operating conditions is analyzed and compared.

Our previous studies have shown that norepinephrine (NE) upregulates proinflammatory cytokines by activating [[alpha].sub.2]-adrenoceptor. Therefore, modulation of the sympathetic nervous system represents a novel treatment for sepsis. We have also shown that a novel stomach-derived peptide, ghrelin, is downregulated in sepsis and that its intravenous administration decreases proinflammatory cytokines and mitigates organ injury. However, it remains unknown whether ghrelin inhibits sympathetic activity through central ghrelin receptors [i.e., growth hormone secretagogue receptor la (GHSR-1a)] in sepsis. To study this, sepsis was induced in male rats by cecal ligation and puncture (CLP). Ghrelin was administered through intravenous or intracerebroventricular injection 30 min before CLP. Our results showed that intravenous administration of ghrelin significantly reduced the elevated NE and TNF-[alpha] levels at 2 h after CLP. NE administration partially blocked the inhibitory effect of ghrelin on TNF-[alpha] in sepsis. GHSR-1a inhibition by the administration of a GHSR-la antagonist, [D-[Arg.sup.1], D-[Phe.sup.5], D-[Trp.sup.7,9], [Leu.sup.11]]substance P, significantly increased both NE and TNF-[alpha] levels even in normal animals. Markedly elevated circulating levels of NE 2 h after CLP were also significantly decreased by intracerebroventricular administration of ghrelin. Ghrelin's inhibitory effect on NE release was completely blocked by intracerebroventricular injection of the GHSR-la antagonist or a neuropeptide Y (NPY)/[Y.sub.1] receptor antagonist. However, ghrelin's downregulatory effect on TNF-[alpha] release was only partially diminished by these agents. Thus ghrelin has sympathoinhibitory properties that are mediated by central ghrelin receptors involving a NPY/Y1 receptordependent pathway. Ghrelin's inhibitory effect on TNF-[alpha] production in sepsis is partially because of its modulation of the overstimulated sympathetic nerve activation. ghrelin; sepsis; sympathetic nervous system; norepinephrine; cytokines