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In recent years, the large-scale construction of subways has caused more and more serious dynamic stray current interference on buried oil and gas pipelines nearby.Effective protection of buried pipelines is necessary to reduce the risk of pipeline corrosion.Because the dynamic fluctuation of subway stray current brings difficulties to the actual test and design of protection scheme, there is still a lack of effective protection design methods under the interference of subway dynamic stray current.In this paper, a buried natural gas pipeline interfered by subway stray current was taken as the research object, and the protection design method based on the field drainage test was explored.Firstly, arranging monitoring points in the interfered pipe section, carrying out detailed 24 h continuous monitoring of dynamic DC interference parameters at multiple interfered locations, and finally analyzing the inflow and outflow laws of subway stray current in the interfered pipe section based on the analysis of monitoring data.On this basis, on-site drainage tests at different locations were carried out, and the subway stray current protection scheme for the interfered pipe section was determined based on on-site tests and related calculations.After the implementation of the scheme, the effect was tested and evaluated, results showed that the expected protection effect was achieved.This work could provide reference for the design of protection scheme for buried pipelines under subway stray current interference.

A Mach-Zehnder interferometer (MZI) sensor based on thin-core fiber (TCF) is proposed. Sensitive materials such as polydimethylsiloxane (PDMS) or gelatin are coated on the surfaces of MZIs to achieve temperature, pressure, and humidity measurements. MZI is composed of single mode fiber (SMF), TCF, and multimode fiber (MMF) spliced together to form a "SMF-MMF-TCF-MMF-SMF" structure. The core/cladding diameters of TCF are 3.8 µm and 80 µm respectively. When three types of optical fibers with different core diameters are cascaded together, many cladding modes are excited to form MZI. Firstly, two similar MZI structures were fabricated designated by MZI1 and MZI2. In order to improve the sensitivity and mechanical strength, a layer of PDMS film was coated on the TCF surface of MZI1. Then, a layer of gelatin film is covered on the TCF surface of MZI2. PDMS has the high thermal expansion coefficient, thermal optical coefficient, and elasticity, and gelatin has good humidity sensitivity properties. The experimental results showed that the temperature and pressure sensitivity of MZI1 coated with PDMS reached −340 pm/°C and −14.3 nm/MPa, respectively, while the humidity sensitivity of MZI2 coated with gelatin reached −112.57 pm/% RH. When a fiber Bragg grating is cascaded with the MZI1, the sensor can achieve simultaneous measurement of temperature and pressure, eliminating crosstalk. The proposed sensor has an extremely simple structure and manufacturing method, which only involves the splicing of optical fiber and the coating by the film. In addition, the proposed sensor has a robust structure, good repeatability and stability, and high sensitivity, which has broad application prospects. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of Qishen decoction on TGR5-mediated activation of NLRP3 inflammasome, so as to clarify the molecular mechanism of its inhibition of macrophage M1-type polarisation to ameliorate non-alcoholic steatohepatitis; Methods: Mouse macrophage cell line RAW264.7 was randomly divided into a control group, model group, Qishen decoction group, TGR5 agonist group and Qishen decoction + TGR5 agonist group. Except for the control group, the remaining groups were constructed the macrophage NLRP3 activation model by palmitic acid induction, and the corresponding drugs were given to intervene. ELISA was used to detect the levels of TNF-α, IL-6, IL-1ß and CXCL2 in macrophage supernatants, flow cytometry was used to detect the expression levels of macrophage polarisation marker molecules CD86 and iNOS, and Western blot was used to detect the expression of the TGR5/STAT1/STAT6 signaling pathway and the expression of NLRP3 inflammasome -associated proteins, respectively. Results: Compared with the control group, the contents of macrophages TNF-α, IL-6, IL-1ß, CXCL2 and the proportion of macrophages with positive expression of CD86 and iNOS were significantly increased in the model group, and the differences were all statistically significant (P<0.01). Compared with the model group, the contents of TNF-α, IL-6, IL-1ß, CXCL2 and the proportion of macrophages with positive expression of CD86 and iNOS were significantly decreased in the Qishen decoction group, and the differences were all statistically significant (P<0.01). In addition, the expression of NLRP3 and Pro-IL-1ß proteins in the macrophage lysate and the expression of Caspase-1 p10, Caspase-1 p20 and IL-1ß p17 proteins in the cell supernatant of the model group were significantly increased when compared with the control group, and the differences were all statistically significant (P<0.01). Compared with the model group, the expression of NLRP3 and Pro-IL-1ß proteins in macrophage lysate and the expression of Caspase-1 p10, Caspase-1 p20 and IL-1ß p17 proteins in cell supernatant of the Qishen decoction were significantly reduced, and the differences were all statistically significant (P<0.01); Conclusion: Qishen decoction can inhibit the activation of NLRP3 inflammasome in macrophages by inhibiting the TGR5/STAT1/STAT6 signaling pathway, thereby inhibiting macrophage M1 polarization and improving inflammatory response. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of Qishen decoction on macrophage polarization mediated by miR-495/FTO signaling pathway, and to clarify the molecular mechanism of Qishen decoction in improving insulin resistance in the treatment of type 2 diabetes. Methods: THP-1 was induced to differentiate macrophages with phorbol ester. It was divided into the control group, the model group, the Qishen decoction group, the miR-495 inhibitor group, and the Qishen decoction+miR-495 inhibitor group. Except for the control group, the remaining groups were stimulated with 30 mmol/L glucose to construct a macrophage polarization model, and corresponding drugs were given for intervention. Cells were collected from each group for 24 hours and the content of inflammatory factors (IL-6, IL-1β, IL-4, and IL-10) were detected using enzyme-linked immunosorbent assay. The expression of macrophage polarization marker molecules, miR-495, and FTO were detected by flow cytometry, qPCR, and Western blot to detect. Results: Compared with the control group, there was no significant change in the activity of macrophages in the control serum, Qishen decoction containing serum, and miR- 495 inhibitor transfected serum, and the difference was not statistically significant (P>0.05). In addition, compared to the control group, the content of IL-6 and IL-1β, the expression levels of CD68, iNOS, COX-2, miR-495, and the ratio of CD68/CD206, were significantly increased (P<0.01). While the content of IL-4 and IL-10, as well as the expression of CD206, Arg-1, YM-1, and FTO were significantly reduced (P<0.01). Compared with the model group, the QiShen decoction significantly reduced the contents of IL-6 and IL-1β, and the expression levels of CD68, iNOS, COX-2, and miR-495, as well as the ratio of CD68/ CD206, while the content of IL-4 and IL-10, as well as the expression of CD206, Arg-1, YM-1, and FTO were significantly increased (P<0.01). Conclusion: Qishen decoction upregulate the expression of FTO to promote M2 type polarization of macrophages, thereby inhibiting inflammation and improving insulin resistance by inhibiting the expression of miR- 495. [ABSTRACT FROM AUTHOR]

Minimally invasive repair strategies are a very promising approach for the treatment of intervertebral disc degeneration (IDD). In recent years, small extracellular vesicles (sEVs) secreted from mesenchymal stem cells (MSCs) have been shown great potential in alleviating IDD. However, in vitro experiments, MSCs are usually exposed to a normoxic micro-environment, which differs greatly from the hypoxic micro-environment in vivo. The primary purpose of our research was to determine whether sEVs isolated from MSCs under hypoxic status (H-sEVs) exhibit a more beneficial effect on protecting IDD compared with sEVs derived from MSCs under normoxic status (N-sEVs). A tail IDD rat model and a series of experiments in vitro were conducted to compare the beneficial effects of PBS, N-sEVs, and H-sEVs treatment. Then, to validate the role of sEVs miRNAs in IDD, a miRNA microarray sequencing analysis and a series of rescue experiments were conducted. Luciferase activity, RNA-ChIP and western blot were performed to explore the potential mechanisms. The results indicate that sEVs alleviate IDD by ameliorating the homeostatic imbalance between anabolism and catabolism in vivo and in vitro. Microarray sequencing result shows that miR-17-5p is maximally enriched in H-sEVs. Toll-like receptor 4 (TLR4) was determined to be a target downstream gene of miR-17-5p. Finally, it was found that H-sEVs miR-17-5p may modulate proliferation and synthesis of human nucleus pulposus cells (HNPCs) matrix via TLR4 pathway. In conclusion, H-sEVs miR-17-5p alleviate IDD via promoting HNPCs matrix proliferation and synthesis, providing new therapeutic targets for IDD. Intervertebral disc degeneration (IDD) is the primary cause of low back pain (LBP), which is a huge burden to society. Our research demonstrates for the first time that hypoxic pretreatment of small extracellular vesicles (H-sEVs) effectively alleviated the progress of IDD. In short, in the present research, we found that H-sEVs miR-17-5p could modulate proliferation and synthesis of nucleus pulposus cells (NPCs) matrix via TLR4/PI3K/AKT pathway. Therefore, hypoxic pre-treatment is a prospective and efficient method to optimize the therapeutic effect of MSCs-derived sEVs. miRNA and MSCs-derived sEVs combination may be a promising therapeutic approach for IDD. [Display omitted] [ABSTRACT FROM AUTHOR]

Targeting cellular senescence and Senescence Associated Secretory Phenotype (SASP) through autophagy has emerged as a promising intervertebral disc (IVD) degeneration (IDD) treatment strategy in recent years. This study aimed to clarify the role and mechanism of autophagy in preventing IVD SASP. Methods involved in vitro experiments with nucleus pulposus (NP) tissues from normal and IDD patients, as well as an in vivo IDD animal model. GATA4's regulatory role in SASP was validated both in vitro and in vivo, while autophagy modulators were employed to assess their impact on GATA4 and SASP. Transcriptomic sequencing identified Oxidized low-density lipoprotein receptor 1 (OLR1) as a key regulator of autophagy and GATA4. A series of experiments manipulated OLR1 expression to investigate associated effects. Results demonstrated significantly increased senescent NP cells (NPCs) and compromised autophagy in IDD patients and animal models, with SASP closely linked to IDD progression. The aged disc milieu impeded autophagic GATA4 degradation, leading to elevated SASP expression in senescent NPCs. Restoring autophagy reversed senescence by degrading GATA4, hence disrupting the SASP cascade. Moreover, OLR1 was identified for its regulation of autophagy and GATA4 in senescent NPCs. Silencing OLR1 enhanced autophagic activity, suppressing GATA4-induced senescence and SASP expression in senescent NPCs. In conclusion, OLR1 was found to control autophagy-GATA4 and SASP, with targeted OLR1 inhibition holding promise in alleviating GATA4-induced senescence and SASP expression while delaying extracellular matrix degradation, offering a novel therapeutic approach for IDD management., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

The production and use of plastic blends have been gradually increasing owing to their versatility and low cost. However, the photodegradation of plastic blends in seawater and the potential risk to the marine environment are still not well understood. In this study, plastic blends including polypropylene/thermoplastic starch blends(PP/TPS) and polylactic acid/poly(butylene adipate-co-terephthalate)/thermoplastic starch blends(PLA/PBAT/TPS) were investigated. The corresponding neat polymers, namely polypropylene(PP) and polylactic acid(PLA), were set as control groups. We investigated the formation of MPs and the changes in the physicochemical properties of plastic blends after photodegradation in seawater. The size distribution of MPs indicated that PP/TPS and PLA/PBAT/TPS were more likely to produce small-sized particles after photodegradation than PP and PLA owing to their poorer mechanical properties and lower resistance to UV irradiation. Noticeable surface morphology alterations, including cracks and wrinkles, were observed for plastic blends following photodegradation, whereas PP and PLA were relatively resistant. After photodegradation, the ATR-FTIR spectrum of PP/TPS and PLA/PBAT/TPS showed a significant decrease in the characteristic bands of thermoplastic starch(TPS), indicating the degradation of their starch fractions. The C 1 s spectra demonstrated that aged plastic blends contained fewer -OH groups than the pristine MPs did, further confirming the photodegradation of TPS. These results indicate that PP/TPS and PLA/PBAT/TPS had a higher degree of photodegradation than PP and PLA and thereby generated more small-sized MPs. In summary, plastic blends may pose a higher risk to the marine environment than neat polymers, and caution should be taken in the production and use of plastic blends.

A Gram-stain-negative, strictly aerobic and rod- to coccoid-shaped bacterium, designated as strain M366 T , was isolated from coastal sediment of Jiaoshanjiao, Zhejiang Province, PR China (121°54' E 29 °38' N). The draft genome of strain M366 T was 3 225 479 bp long (with 55.6 mol% G+C content) and assembled into four contigs. The N50 value was 563 270 bp and the genomic completeness and contamination were estimated to be 99.34 and 0.05 %, respectively. Colonies of strain M366 T were yellow-orange, 1 mm in diameter, round, opaque, smooth and convex after incubation on marine agar at 30 °C for 3 days. Cells were catalase-positive but oxidase-negative. Strain M366 T was observed to grow at 20-40 °C (optimum, 30 °C), pH 5.5-9.0 (optimum, pH 6.5-7.0) and with 0.5-8.0 % (w/v) NaCl (optimum, 2.5 %). Strain M366 T shown highest 16S rRNA gene sequence similarity of 98.1 % to Robiginitalea sediminis O458 T , 95.6-95.9 % to other type strains of the genus Robiginitalea and below 93 % to other genera. The average nucleotide identity and digital DNA-DNA hybridization values between strain M366 T and its closely related Robiginitalea species were 71.1-75.9 % and 17.5-19.0 %. Menaquinone-6 was the only respiratory quinone. The major fatty acids (>10 %) were iso-C 15 : 0 , iso-C 17 : 0 3-OH and summed feature 1 (iso-C 15 : 1  h and/or C 13 : 0 3-OH). The main polar lipids included phosphatidylethanolamine, two unidentified phospholipid, two unidentified aminophospholipid, one unidentified glycolipid and five unidentified lipids. According to the above results, Robiginitalea aestuariiviva sp. nov. is proposed and the type strain is M366 T (=KCTC 92866 T =MCCC 1K04524 T =CGMCC 1.61708 T ).