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In this study, the electrochemical softening method was used to treat the simulated drainage of the converter station, and the treatment effect under different water inlet conditions was investigated. The results show that the hardness removal rate is from 10% to 80% when the residence time is from 0.5h to 4h, and the longer the residence time is, the higher the removal rate is. The maximum scale removal capacity reached 2.67g/h/m2 when residence time was 1h. Through the formula fitting of several groups of tests, it is concluded that the removal effect can be expressed by the formula C0/C=0.9627e(17.73at/V) under different water intake (residence time).

Background: Neuronal abnormalities are closely associated with major depressive disorder (MDD). Available evidence suggests a role for microRNAs (miRNAs) in regulating the expression of genes involved in MDD. Hence, miRNAs that can be potential therapeutic targets need to be identified. Methods: A mouse model of chronic unpredictable stress (CUS) was used to evaluate the function of miRNAs in MDD. miR‐144‐5p was screened from the hippocampi of CUS mice based on sequencing results. Adenovirus‐associated vectors were used to overexpress or knockdown miR‐144‐5p in mice. BpV(pic) and LY294002 were used to determine the relationship between miR‐144‐5p target genes PTEN and TLR4 in neuronal impairment caused by miR‐144‐5p deficiency. Western blotting, immunofluorescence, ELISA immunosorbent assay, and Golgi staining were used to detect neuronal abnormalities. Serum samples from healthy individuals and patients with MDD were used to detect miR‐144‐5p levels in the serum and serum exosomes using qRT‐PCR. Results: miR‐144‐5p expression was significantly decreased within the hippocampal dentate gyrus (DG) of CUS mice. Upregulation of miR‐144‐5p in the DG ameliorated depression‐like behavior in CUS mice and attenuated neuronal abnormalities by directly targeting PTEN and TLR4 expression. Furthermore, miR‐144‐5p knockdown in normal mice led to depression‐like behavior via inducing neuronal abnormalities, including abnormal neurogenesis, neuronal apoptosis, altered synaptic plasticity, and neuroinflammation. miR‐144‐5p deficiency‐mediated neuronal impairment was mediated by PI3K/Akt/FoxO1 signaling. Furthermore, miR‐144‐5p levels were downregulated in the sera of patients with MDD and associated with depressive symptoms. Consistently, serum exosome‐derived miR‐144‐5p levels were decreased in patients with MDD. Conclusion: miR‐144‐5p plays a vital role in regulating neuronal abnormalities in depression. Our findings provide translational evidence that miR‐144‐5p is a new potential therapeutic target for MDD. [ABSTRACT FROM AUTHOR]

The Madeng hot spring emerges in the central river valley in the northeastern Lanping Basin in Jianchuan county of Yunnan Province in China. Quaternary sand and gravel occur in the valley which is underlain by the red beds consisting of sandstone and mudstone. The temperature of the hot spring is 42.1°C. The spring water has a pH value of 6.41, TDS of 3.98 g/L, F contents of 3.08 mg/L, and H2SiO3 of 35.6 mg/L. The hot water is of SO4•Cl-Na•Ca type. There is a slight hydrogen sulfide odor in the spring water. Stable hydrogen and oxygen isotopes indicate that the hot water is of meteoric origin. It is estimated that the elevation of the recharge area of the hot spring is approximately 3800 m, the age of the hot water is some 140 years, the temperature of the geothermal reservoir is 75°C–80°C, the mixture ratio of cold water is approximately 80%, and the circulation depth of the thermal groundwater is 1870 m. After receiving recharge from infiltration of precipitation in the mountainous recharge areas, the groundwater undergoes a deep circulation, obtains heat from the heat flow, flows upward along the fractured zone, and emerges as an upflow spring through the Quaternary sand and gravel in the central low-lying river valley.

In order to obtain conductive concrete with good electrical conductivity and good mechanical properties, nanographite and magnetite sand excited by different activators and their combinations are added to ordinary concrete to obtain high quality and efficient conductive concrete. The optimal mixture ratio of alkali-excited conductive concrete and the effects of different activators and their combinations on the mechanics and electrical conductivity of concrete were studied. The microstructure of alkali-excited conductive concrete was analyzed by scanning electron microscope (SEM) to study its conductive mechanism. Results show that the conductive concrete obtained by compounding sodium hydroxide, sodium sulfate and calcium hydroxide has optimal mechanical and electrical properties when the graphite is 6% cement, and magnetite sand is 40% fine aggregate. The conductive concrete sample prepared by this method has a flexural strength of 6.84 MPa, a compressive strength of 47.79 MPa and a resistivity of 4805 Ω·cm (28 days). Compared with ordinary concrete (no nanographite and no magnetite sand), the compressive strength of conductive concrete is increased by 122.3%, the bending strength is increased by 116.5%, and the resistivity is reduced by 99.1%. SEM shows that the distribution of conductive materials in concrete is more uniform due to alkali excitation and calcium silicate hydrate (CSH) gel can be formed, which leads to better performance. The research in this paper is only a preliminary exploration of the characteristics of green conductive concrete, and the conductive heating characteristics and electromagnetic wave absorption properties of concrete, along with strength characteristics after adding conductive fillers, need to be further studied. It is suggested that further research should be carried out on the deicing characteristics of conductive concrete and the electromagnetic wave absorption properties used in stealth military engineering. [ABSTRACT FROM AUTHOR]

Targeting Treg cells: Depletion of regulatory T (Treg) cells is an attractive strategy to promote antitumor immunity. One strategy that could deplete Treg cells is blockade of the "do not eat me" signal, CD47, which prevents Treg cells from being targets of phagocytosis. However, CD47 is broadly expressed, making Treg cell–specific targeting difficult. To selectively deplete Treg cells, Zhang et al. designed a heterodimer that combines an anti–cytotoxic T lymphocyte antigen 4 (CTLA-4) antibody, which targets intratumoral Treg cells, and the CD47 ligand, signal regulatory protein α (SIRPα). Treatment with this heterodimer increased phagocytosis of Treg cells, leading to their depletion, and promoted antitumor immunity in mouse models. Thus, dual targeting of CD47 and CTLA-4 selectively depletes Treg cells and can promote immune responses against solid tumors. Blockade of CD47, the "do not eat me" signal, has limited effects in solid tumors despite its potent antitumor effects in hematopoietic malignancies. Taking advantage of the high expression of cytotoxic T lymphocyte–associated protein 4 (CTLA-4) on Treg cells and abundant Fc receptor–expressing active phagocytes inside the tumor microenvironment (TME), we designed and tested a heterodimer combining an anti–CTLA-4 antibody, which targets Treg cells, with the CD47 ligand, signal regulatory protein α (SIRPα), to selectively block CD47 on intratumoral Treg cells. We hypothesized that heterodimer treatment would increase antibody-dependent cellular phagocytosis of the targeted Treg cells. We found that anti–CTLA-4×SIRPα preferentially depleted ICOShigh immunosuppressive Treg cells in the TME and enhanced immunity against solid tumors, including MC38 and CT26 murine colon cancers. Mechanistically, we found that CD47 expression on Treg cells limited anti–CTLA-4–mediated depletion and Fc on the heterodimer-enhanced depletion. Furthermore, anti-human CTLA-4×SIRPα depleted tumor Treg cells and exhibits less toxicity than anti-human CTLA-4 in a humanized mouse model. Collectively, these results demonstrate that simultaneously modulating both "eat me" and do not eat me signals induces Treg cell depletion inside the TME and may be an effective strategy for treating solid tumors. [ABSTRACT FROM AUTHOR]