[This corrects the article DOI: 10.3389/fbioe.2021.691091.].

Acute lung injury (ALI) is a critical pulmonary condition characterized by high morbidity and mortality rates. Recent studies have highlighted the therapeutic potential of engineered exosomes derived from mesenchymal stem cell (MSC) in modulating the inflammatory response in ALI. Here, a novel approach was developed to fabricate engineered bone mesenchymal stem cells (BMSCs) derived exosomes by utilizing superparamagnetic iron oxide nanoparticles (SPIONs) and an alternating magnetic field (AMF) to precondition BMSCs. This study evaluated and compared the therapeutic potential of different groups of engineered exosomes in ALI mice model and analyzed their underlying mechanisms using high-throughput sequencing. BMSCs were isolated from SD rats and subjected to treatment with SPIONs and/or an AMF. Following this, we established a lipopolysaccharide (LPS)-induced ALI mice model and evaluated the therapeutic efficacy of exosomes from different groups by administering them via tail vein injection. The expression profiles of microRNAs (miRNAs) in exosomes were compared to explore the mechanism of regulating inflammatory response and ameliorating lung injury. 25 µg/mL SPIONs and 3mT AMF were the best conditions for preparing engineered exosomes, which reduced the level of pro-inflammatory factors and had the most significant effect in repaired lung damage in vivo. The transfection of miR-145-5p mimics enhanced Bronchial Epithelium transformed with Ad12-SV40 2B (BEAS-2B) cells viability and reduced relevant inflammation expression in vitro experiments. The engineered exosomes obtained by low dose SPIONs combined with AMF can help regulate the level of inflammatory factors and improve lung injury. Targeted regulation of kruppel-like factor 5 (KLF5) by exosomal miR-145-5p and inhibition of the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway play a key role in this vitro process.

Purpose: Treatment for bone and joint tuberculosis (BJTB) is challenging due to its refractory and recurrent nature. This study aimed to develop a bioimplantable scaffold with osteoinductive and antituberculosis characteristics to treat BJTB. Methods: This scaffold is built on oxidized hyaluronic acid and carboxymethyl chitosan hydrogel mixed with hydroxyapatite as a bone tissue engineered material. In order to make the scaffold have the biological activity of promoting tissue repair, the engineered exosomes (Exoeng) were added innovatively. In addition, drug-loaded liposomes equipped with an aldehyde group on the surface are cross-linked with the amine group of the hydrogel skeleton to participate in the Schiff base reaction. Results: The designed scaffold has characteristics of self-healing and injectability exhibit excellent anti-tuberculosis and promoting bone repair activities. Exoeng strongly stimulates cellular angiogenesis and osteogenic differentiation. The liposomes coated in hydrogel can release three kinds of anti-tuberculosis drugs smoothly and slowly, achieving a long term anti-tuberculosis. Conclusion: The composite bio-scaffold shows good tissue repair and long-term anti-tuberculosis abilities, which expected to provide a viable treatment plan for bone-related BJTB.

Ferroptosis, a unique iron-dependent mode of cell death characterized by lipid peroxide accumulation, holds significant potential for the treatment of glioblastoma (GBM). However, the effectiveness of ferroptosis is hindered by the limited intracellular ferrous ions (Fe2+) and hydrogen peroxide (H2O2). In this study, a novel near-infrared (NIR)-light-responsive nanoplatform (ApoE-UMSNs-GOx/SRF) based on upconversion nanoparticles (UCNPs) was developed. A layer of mesoporous silica and a lipid bilayer were coated on UCNPs sequentially and loaded with glucose oxidase (GOx) and sorafenib, respectively. Further attachment of the ApoE peptide endowed the nanoplatform with BBB penetration and GBM targeting capabilities. Our results revealed that ApoE-UMSNs-GOx/SRF could efficiently accumulated in the orthotopic GBM and induce amplified ferroptosis when combining with NIR irradiation. The UCNPs mediated the photoreduction of Fe3+ to Fe2+ by converting NIR to UV light, and excess H2O2 was produced by the reaction of glucose with the loaded GOx. These processes greatly promoted the production of ROS, which together with inhibition of system Xc- by the loaded sorafenib, leading to enhanced accumulation of lipid peroxides and significantly improved the antiglioma effect both in vitro and in vivo. Our strategy has the potential to enhance the effectiveness of ferroptosis as a therapeutic approach for GBM.

Subarachnoid hemorrhage (SAH) is primarily attributed to the rupture of intracranial aneurysms and is associated with a high incidence of disability and mortality. SAH disrupts the blood‒brain barrier, leading to the release of iron ions from blood within the subarachnoid space, subsequently inducing neuronal ferroptosis. A recently discovered protein, known as ferroptosis suppressor protein 1 (FSP1), exerts anti-ferroptotic effects by facilitating the conversion of oxidative coenzyme Q 10 (CoQ10) to its reduced form, which effectively scavenges reactive oxygen radicals and mitigates iron-induced ferroptosis. In our investigation, we observed an increase in FSP1 levels following SAH. However, the depletion of CoQ10 caused by SAH hindered the biological function of FSP1. Therefore, we created neuron-targeted liposomal CoQ10 by introducing the neuron-targeting peptide Tet1 onto the surface of liposomal CoQ10. Our objective was to determine whether this formulation could activate the FSP1 system and subsequently inhibit neuronal ferroptosis. Our findings revealed that neuron-targeted liposomal CoQ10 effectively localized to neurons at the lesion site after SAH. Furthermore, it facilitated the upregulation of FSP1, reduced the accumulation of malondialdehyde and reactive oxygen species, inhibited neuronal ferroptosis, and exerted neuroprotective effects both in vitro and in vivo. Our study provides evidence that supplementation with CoQ10 can effectively activate the FSP1 system. Additionally, we developed a neuron-targeted liposomal CoQ10 formulation that can be selectively delivered to neurons at the site of SAH. This innovative approach represents a promising therapeutic strategy for neuronal ferroptosis following SAH.Statement of SignificanceSubarachnoid hemorrhage (SAH) is primarily attributed to the rupture of intracranial aneurysms and is associated with a high incidence of disability and mortality. Ferroptosis suppressor protein 1 (FSP1), exerts anti-ferroptotic effects by facilitating the conversion of oxidative coenzyme Q 10 (CoQ10) to its reduced form, which effectively scavenges reactive oxygen radicals and mitigates iron-induced ferroptosis. In our investigation, we observed an increase in FSP1 levels following SAH. However, the depletion of CoQ10 caused by SAH hindered the biological function of FSP1. Therefore, we created neuron-targeted liposomal CoQ10. We find that it effectively localized to neurons at the lesion site after SAH and activated the FSP1/CoQ10 system. This innovative approach represents a promising therapeutic strategy for neuronal ferroptosis following SAH and other central nervous system diseases characterized by disruption of the blood-brain barrier.

Ferroptosis, a unique iron-dependent mode of cell death, has been identified as a potential treatment for glioblastoma (GBM). Dihydroartemisinin (DHA) is a ferroptosis inducer with cytotoxicity that is strongly dependent on intracellular Fe2+ levels. However, the effectiveness of DHA is limited by low levels of Fe2+ in tumor cells. To address this issue, a facile strategy was developed by combining near-infrared (NIR)-induced ferrous ion regeneration with DHA in a nanocomposite (ApoE-UPGs-DHA). This nanocomposite synergistically enhanced ferroptosis and offered highly efficient GBM treatment. ApoE-UPGs-DHA were prepared by loading upconversion nanoparticles (UCNPs) and DHA into micelles and subsequently attaching the peptide apolipoprotein E to enable penetration of the blood-brain barrier (BBB) and targeted treatment of GBM. NIR irradiation was applied to induce the regeneration of Fe2+ from Fe3+ mediated by ApoE-UPGs-DHA, thereby promoting ferroptosis in G422 glioma cells. Characterization studies confirmed the successful preparation of ApoE-UPGs-DHA, which had a diameter of 82.3 +/- 5.8 nm. The nanocomposite demonstrated good GBM targeting ability in vivo and enhanced uptake by the G422 cells in vitro. ApoE-UPGs-DHA were toxic to G422 glioma cells, and this toxicity was further enhanced by NIR irradiation. Mechanistic studies revealed that ApoE-UPGs-DHA treatment led to a decrease in the intracellular Fe2+ concentration due to the Fenton-like reaction induced by DHA and Fe2+. NIR irradiation was transformed into UV light by ApoE-UPGs-DHA, and then, the Fe3+ generated by the Fenton reaction was photoreduced to Fe2+ by UV light. The replenished Fe2+ significantly promoted the generation of lipid peroxides (LPOs), leading to enhanced ferroptosis and toxicity to ApoE-UPGs-DHA-treated G422 glioma cells. Herein, an NIR-responsive Fe2+-regenerating nanocomposite was successfully prepared to enhance ferroptosis in G422 glioma cells, suggesting a promising alternative GBM treatment strategy.

Aged cells have a reduced ability to regenerate tissues. Thus, it is intriguing to reactivate the adult cells to regenerate. Here, we used hair follicles as a model to study how mechanical stimuli induce hair regeneration using hair plucking and organoid culture approaches in adult mice. We observed that skin organoid cultures using cells derived from day 3 post-plucking (PPD3) skin had the highest hair regeneration capacity. The regenerated hair follicles had normal morphology. By RNA-sequencing, single-cell RNA-sequencing analysis, and in situhybridization, we identified that the chemokine signaling pathway genes including Ccl2 are significantly increased in the hair follicle and surrounding dermal microenvironment at PPD3, as well as in skin organoid cultures. Immunostaining shows that the PPD3 skin epithelial cells have increased multipotency. Under organoid culture, these skin cells can self-organize to form epidermal aggregates. By adding CCL2 recombinant protein to the skin organoid culture using an environmental reprogramming protocol, we observed the adult cells which lose their regenerative ability can self-organize in organoid culture and regenerate hair follicles upon transplantation. In summary, we elucidate the mechanism by which mechanical stimulus induces hair regeneration at the microenvironmental regulation level using the hair plucking and organoid culture models. Our study reinforces the concept of immune regulation in hair regeneration under mechanical stimuli. The immune modulation in the skin organoid culture system also provides therapeutic potential for future clinical application.

Currently, the treatment of triple-negative breast cancer (TNBC) is limited by the special pathological characteristics of this disease. In recent years, photodynamic therapy (PDT) has created new hope for the treatment of TNBC. Moreover, PDT can induce immunogenic cell death (ICD) and improve tumor im-munogenicity. However, even though PDT can improve the immunogenicity of TNBC, the inhibitory im-mune microenvironment of TNBC still weakens the antitumor immune response. Therefore, we used the neutral sphingomyelinase inhibitor GW4869 to inhibit the secretion of small extracellular vesicles (sEVs) by TNBC cells to improve the tumor immune microenvironment and enhance antitumor immunity. In ad-dition, bone mesenchymal stem cell (BMSC)-derived sEVs have good biological safety and a strong drug loading capacity, which can effectively improve the efficiency of drug delivery. In this study, we first ob-tained primary BMSCs and sEVs, and then the photosensitizers Ce6 and GW4869 were loaded into the sEVs by electroporation to produce immunomodulatory photosensitive nanovesicles (Ce6-GW4869/sEVs). When administered to TNBC cells or orthotopic TNBC models, these photosensitive sEVs could specif-ically target TNBC and improve the tumor immune microenvironment. Moreover, PDT combined with GW4869-based therapy showed a potent synergistic antitumor effect mediated by direct killing of TNBC and activation of antitumor immunity. Here, we designed photosensitive sEVs that could target TNBC and regulate the tumor immune microenvironment, providing a potential approach for improving the effec-tiveness of TNBC treatment.Statement of Significance We designed an immunomodulatory photosensitive nanovesicle (Ce6-GW4869/sEVs) with the photosensi-tizer Ce6 to achieve photodynamic therapy and the neutral sphingomyelinase inhibitor GW4869 to inhibit the secretion of small extracellular vesicles (sEVs) by triple-negative breast cancer (TNBC) cells to improve the tumor immune microenvironment and enhance antitumor immunity. In this study, the immunomodulatory photosensitive nanovesicle could target TNBC cells and regulate the tumor immune microenvi-ronment, thus providing a potential approach for improving the treatment effect in TNBC. We found that the reduction in tumor sEVs secretion induced by GW4869 improved the tumor-suppressive immune mi-croenvironment.

Background:Central nervous system tuberculosis (CNS-TB) is the most devastating form of extrapulmonary tuberculosis. Rifampin (RIF) is a first-line antimicrobial agent with potent bactericidal action. Nonetheless, the blood-brain barrier (BBB) limits the therapeutic effects on CNS-TB. Exosomes, however, can facilitate drug movements across the BBB. In addition, exosomes show high biocompatibility and drug-loading capacity. They can also be modified to increase drug delivery efficacy. In this study, we loaded RIF into exosomes and modified the exosomes with a brain-targeting peptide to improve BBB permeability of RIF; we named these exosomes ANG-Exo-RIF.Methods:Exosomes were isolated from the culture medium of BMSCs by differential ultracentrifugation and loaded RIF by electroporation and modified ANG by chemical reaction. To characterize ANG-Exo-RIF, Western blot (WB), nanoparticle tracking analysis (NTA) and transmission electron microscopy (TEM) were performed. Bend.3 cells were incubated with DiI labeled ANG-Exo-RIF and then fluorescent microscopy and flow cytometry were used to evaluate the targeting ability of ANG-Exo-RIF in vitro. Fluorescence imaging and frozen section were used to evaluate the targeting ability of ANG-Exo-RIF in vivo. MIC and MBC were determined through microplate alamar blue assay (MABA).Results:A novel exosome-based nanoparticle was developed. Compared with untargeted exosomes, the targeted exosomes exhibited high targeting capacity and permeability in vitro and in vivo. The MIC and MBC of ANG-Exo-RIF were 0.25 μg/mL, which were sufficient to meet the clinical needs.Conclusion:In summary, excellent targeting ability, high antitubercular activity and biocompatibility endow ANG-Exo-RIF with potential for use in future translation-aimed research and provide hope for an effective CNS-TB treatment.

Hepatocellular carcinoma (HCC) is common worldwide, and novel therapeutic targets and biomarkers are needed to improve outcomes. In this study, bioinformatics analyses combined with in vitro and in vivo assays were used to identify the potential therapeutic targets. Differentially expressed genes (DEG) in HCC were identified by the intersection between The Cancer Genome Atlas and International Cancer Genome Consortium data. The DEGs were evaluated by a gene set enrichment analysis as well as Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. A protein interaction network, univariate Cox regression, and Lasso regression were used to screen out hub genes correlated with survival. Increased expression of the long noncoding RNA GBAP1 in HCC was confirmed in additional datasets and its biological function was evaluated in HCC cell lines and nude mice. Among 121 DEGs, GBAP1 and PRC1 were identified as hub genes with significant prognostic value. Overexpression of GBAP1 in HCC was confirmed in 21 paired clinical tissues and liver cancer or normal cell lines. The inhibition of GBAP1 expression reduced HCC cell proliferation and promoted apoptosis by inactivating the PI3K/AKT pathway in vitro and in vivo. Therefore, GBAP1 has a pro-oncogenic function in HCC and is a candidate prognostic biomarker and therapeutic target.

OBJECTIVE:To investigate the survival outcomes and risk factors for mortality in cirrhotic patients with probable spontaneous bacterial peritonitis (SBP). METHODS:We retrospectively analyzed the clinical data of 323 cirrhotic patients with ascites admitted from June 2021 to May 2022, including 115 patients with SBP [ascites polymorphonuclear leucocyte (PMN) count ≥250/mm3], 52 patients with bacterascites (PMN count < 250/mm3 with positive microbiological finding in ascites), 67 patients with probable SBP (PMN count < 250/mm3 with negative microbiological finding in ascites but clinical symptoms of SBP) and 89 patients without infection (PMN count < 250/mm3 with negative microbiological finding without clinical symptoms of SBP). The clinical characteristics, laboratory data and 90-day mortality of the patients were compared among the 4 groups. Cox proportional hazard model and propensity score matching (PSM) in a 1∶1 ratio were used to analyze the risk factors for mortality in patients with probable SBP. RESULTS:The patients with probable SBP had a 90-day mortality rate of 43.28%, similar to those of patients with SBP (46.95%, P=0.121) and bacterascites (48.07%, P=0.805) but significantly higher than that of non-infected patients (11.23%, P < 0.001). In the 46 pairs of patients matched using PSM, the 90-day mortality rates were higher in probable SBP group than in non-infected group both before (43.28% vs 11.23%, P < 0.001) and after PSM (34.78% vs 15.21%, P=0.038). Cox regression analysis indicated that probable SBP was an independent predictor of 90-day mortality in cirrhotic patients with ascites (HR=1.539, 95% CI: 1.048-2.261, P=0.028). A Model for End-Stage Liver Disease (MELD) score > 15 (HR=1.943, 95% CI: 1.118-3.377, P=0.018) and procalcitonin level > 0.48 ng/mL (HR=1.989, 95% CI: 1.111-3.560, P=0.021) at diagnostic paracentesis were both independent risk factors for 90-day mortality in patients with probable SBP. CONCLUSION:Cirrhotic patients with probable SBP have poor survival outcomes, and their management should be further optimized based on their MELD score and procalcitonin level.

Background Radiation therapy (RT) is commonly used to treat glioblastoma, but its immunomodulatory effect on tumors, through mechanisms such as immunogenic cell death (ICD), is relatively weak. Gold nanoparticles (AuNPs) have been suggested as potential radio-sensitizers, but it is unclear if they can enhance radiation-induced ICD. This study aimed to investigate the potential of AuNPs to improve the effectiveness of radiation-induced ICD. Methods G422 cells were treated with a combination of AuNPs and RT to induce cell death. Various assays were conducted to assess cell death, surface expression of CRT, and release of HMGB1 and ATP. In vitro co-culture experiments with bone marrow-derived dendritic cells (BMDCs) were performed to analyze the immunogenicity of dying cancer cells. Flow cytometry was used to measure the maturation rate of BMDCs. An in vivo mouse tumor prophylactic vaccination model was employed to assess immunogenicity. Results The study findings presented here confirm that the combination of radiotherapy (RT) with AuNPs can induce a stronger ICD effect on glioblastoma cells compared to using RT alone. Specifically, treatment with AuNPs combined with RT resulted in the emission of crucial damage-associated molecular patterns (DAMPs) such as CRT, HMGB1 (479.41±165.34pg/mL vs 216.04±178.16 pg/mL, *P<0.05) and ATP (The release of ATP in the AuNPs + RT group was 1.2 times higher than in the RT group, *P<0.05). The proportion of BMDC maturation rate was higher in the group treated with AuNPs and RT compared to the group treated with RT alone. (32.53±0.52% vs 25.03±0.28%,***P < 0.001). In the tumor vaccine experiment, dying tumor cells treated with AuNPs and RT effectively inhibited tumor growth in mice when exposed to living tumor cells. Conclusion These results indicate that AuNPs have the ability to enhance RT-induced ICD.

Background:Cancers trigger systemic metabolic disorders usually associated with glucose intolerance, which is an initially apparent phenomenon. One of the features of pancreatic cancer (PC) metabolic reprogramming is the crosstalk between PC and peripheral tissues (skeletal muscle and adipose tissues), emphasized by insulin resistance (IR). Our previous study reported that mice pancreatic cancer-derived exosomes could induce skeletal muscle cells (C2C12) IR, and exosomal microRNAs (miRNAs) may exert an important effect. However, the underlying mechanism remains to be further elucidated.Methods:qPCR was used to determine the expression of let-7b-5p in normal pancreatic islet cells and PC cells. Exosomes were purified from PC cell culture medium by ultracentrifugation. The role let-7b-5p on IR-mediated by PC cells-derived exosomes was asses by Oil Red O staining using miRNA inhibitor. Western blot assay was performed to examine the expression of IR-related genes and the activation of signaling pathways. A Luciferase experiment was applied to confirm how let-7b-5p regulated the expression of RNF20. IP/WB analysis further determined whether RNF20 promoted STAT3 ubiquitination. Rescue experiment using RNF20 overexpression plasmid was performed to confirm the role of RNF20 on IR-mediated using PC cell-derived exosomes in C2C12 myotube cells.Results:miRNA-let-7b-5p was identified as the key exosomal miRNA, which could promote the IR in C2C12 myotube cells supported the lipid accumulation, the activation of STAT3/FOXO1 axis, and the decreased expression of IRS-1 and GLUT4. RNF20, an E3 ubiquitin ligase, was confirmed as the target gene of let-7b-5p and was found to improve IR by downregulating STAT3 protein expression via ubiquitination-mediated protein degradation. The ectopic expression of RNF20 could effectively attenuate the IR mediated by the pancreatic cancer-derived exosomes in C2C12 myotube cells.Conclusion:Our data suggest that exosomal miRNA-let-7b-5p may promote IR in C2C12 myotube cells by targeting RNF20 to activate the STAT3/FOXO1 axis.

Abstract. In this paper we develop a novel framework aimed to significantly reduce biases related to marine stratocumulus clouds in general circulation models (GCMs) while circumventing excessive computational cost requirements. Our strategy is to increase the horizontal resolution using a regionally refined mesh (RRM) over our region of interest in addition to using the Framework for Improvement of Vertical Enhancement (FIVE) to increase the vertical resolution only for specific physical processes that are important for stratocumulus. We apply the RRM off the coast of Peru in the Southeast Pacific, a region that climatologically contains the most marine stratocumulus in the subtropics. We find that our new modeling framework is able to replicate the results of our high resolution benchmark simulation with much fidelity, while reducing the computational cost by several orders of magnitude. In addition, this framework is able to greatly reduce the longstanding biases associated with marine stratocmulus in GCMs when compared to the standard resolution control simulation.

Gastrointestinal cancer (GIC) is the most common cancer with a poor prognosis. Currently, surgery is the main treatment for GIC. However, the high rate of postoperative recurrence leads to a low five-year survival rate. In recent years, immunotherapy has received much attention. As the only immunotherapy drugs approved by the Food and Drug Administration (FDA), immune checkpoint blockade (ICB) drugs have great potential in cancer therapy. Nevertheless, the efficacy of ICB treatment is greatly limited by the low immunogenicity and immunosuppressive microenvironment of GIC. Therefore, the targets of immunotherapy have expanded from ICB to increasing tumor immunogenicity, increasing the recruitment and maturation of immune cells and reducing the proportion of inhibitory immune cells, such as M2-like macrophages, regulatory T cells and myeloid-derived suppressor cells. Moreover, with the development of nanotechnology, a variety of nanoparticles have been approved by the FDA for clinical therapy, so novel nanodrug delivery systems have become a research focus for anticancer therapy. In this review, we summarize recent advances in the application of immunotherapy-based nanoparticles in GICs, such as gastric cancer, hepatocellular carcinoma, colorectal cancer and pancreatic cancer, and described the existing challenges and future trends.

Hepatocellular carcinoma is the third most common cause of cancer-related deaths in China and immune-based therapy can improve patient outcomes. In this study, we investigated the relationship between immunity-associated genes and hepatocellular carcinoma from the prognostic perspective. The data downloaded from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) and the Gene Expression Omnibus (GEO) was screened for gene mutation frequency using the maftools package. Immunity-associated eight-gene signature with strong prognostic ability was constructed and proved as an independent predictor of the patient outcome in LIHC. Seven genes in the immune-related eight-gene signature were strongly associated with the infiltration of M0 macrophages, resting mast cells, and regulatory T cells. Our research may provide clinicians with a quantitative method to predict the prognosis of patients with liver cancer, which can assist in the selection of the optimal treatment plan.

背景:现有的外泌体蛋白组学研究中,只有不同来源外泌体或者不同条件下分泌的外泌体之间的蛋白组学对比,没有外泌体和其母体细胞之间的对比分析.目的:对人脐带间充质干细胞来源外泌体进行提取鉴定和蛋白组学分析.方法:培养人脐带间充质干细胞并采用超滤序贯超离法提取外泌体,通过透射电镜、纳米颗粒跟踪分析、蛋白质定量、蛋白质印迹法及蛋白组学分析等技术鉴定.结果 与结论:①提取的外泌体分散度较好且均一,多为杯状圆形或类圆形的膜性小囊泡,可见囊泡的双膜性结构,中央为低电子密度成分,分布较集中且边界清晰;②外泌体粒径分布峰值为(129.5±8.7)nm,膜表面带负电荷,浓度为8.375×1010粒子/mL,平均zeta电位为(-28.1±3.6)mV;③外泌体有特征性膜蛋白CD9、CD63的表达;④蛋白组学分析外泌体中高表达的蛋白质大多参与RNA剪接、mRNA加工、蛋白折叠等生物过程,参与RNA/DNA等遗传物质及蛋白质的合成、加工、降解过程,参与组成多种细胞器及亚细胞膜结构,参与多条信号通路、细胞黏附、细胞外基质受体相互作用,与多种疾病和病毒致癌也密切相关;⑤通过分析认为外泌体与其母体细胞相比有一定的同质性和差异性,差异蛋白功能均和免疫无关,故验证了人脐带间充质干细胞来源外泌体的低免疫原性和安全性.

Radon and radon daughters pose significant backgrounds to rare-event searching experiments. Activated carbon, which has very strong adsorption capacity for radon, can be used for radon removal and radon enrichment. The internal $^{226}$Ra concentration ultimately limits its radon enrichment ability. In order to measure the intrinsic background and study the radon adsorption capability of Saratech activated carbon at various temperatures, a radon-emanation measurement system with a high-sensitivity radon detector and an adsorption-performance research-system have been developed. In this paper, a 0.71~mBq/m$^3$ high-sensitivity radon detector and measurement details of the radon-adsorption capability of Saratech activated carbon at low temperature will be presented.