Inverted loading strategy regulates the Mn-OV-Ce sites for efficient fenton-like catalysis.

Regulating interfacial active sites to improve peroxymonosulfate (PMS) activation efficiency is a hot topic in the heterogeneous catalysis field. In this study, we develop an inverted loading strategy to engineer asymmetric Mn-OV-Ce sites for PMS activation. Mn3O4@CeO2 prepared by loading CeO2 nanoparticles onto Mn3O4 nanorods exhibits the highest catalytic activity and stability, which is due to the formation of more oxygen vacancies (OV) at the Mn-OV-Ce sites, and the surface CeO2 layer effectively inhibits corrosion by preventing the loss of manganese ion active species into the solution. In situ characterizations and density functional theory (DFT) studies have revealed effective bimetallic redox cycles at asymmetric Mn-OV-Ce active sites, which promote surface charge transfer, enhance the adsorption reaction activity of active species toward pollutants, and favor PMS activation to generate (•OH, SO4•-, O2•- and 1O2) active species. This study provides a brand-new perspective for engineering the interfacial behavior of PMS activation.

Disulfidptosis and ferroptosis related genes predict prognosis and personalize treatment for hepatocellular carcinoma.

Background: Understanding the interplay between disulfidptosis, ferroptosis, and hepatocellular carcinoma (HCC) could provide valuable insights into the pathogenesis of HCC and potentially identify novel therapeutic targets for the treatment of this deadly disease. This study aimed to identify a prognostic signature for HCC by examining the differential expression of genes related to disulfidptosis and ferroptosis (DRG-FRG), and to assess its clinical applicability. Methods: By integrating 23 disulfidptosis and 259 ferroptosis related genes with HCC messenger RNA (mRNA) expression data from The Cancer Genome Atlas (TCGA), differentially expressed DRG-FRG genes were identified. From these, 11 DRG-FRG genes were selected to construct a risk signature model using least absolute shrinkage and selection operator regression analyses. The prognostic performance of this model was evaluated by Kaplan-Meier survival analysis and time-dependent receiver operating characteristic (ROC) analysis. Subsequently, a nomogram was built by combining the signature with clinical variables. To further delve into the underlying mechanisms, we performed bioinformatics analysis using a variety of databases. Results: A prognostic signature based on 11 DRG-FRG genes effectively categorized HCC patients into high- and low-risk groups, showing a significant survival difference. Even after considering clinical variables, this signature remained an independent prognostic factor. Furthermore, the signature played a role in various critical biological processes and pathways that drive HCC progression. Potential therapeutic benefits could be derived from small molecule drugs targeting NQO1 and SLC7A11. Interestingly, the high-risk group exhibited resistance to several chemotherapeutic drugs, yet showed sensitivity to others when contrasted with the low-risk group. Lastly, the DRG-FRG genes signature had a strong correlation with the tumor immune microenvironment, marked by an elevated expression of immune checkpoint molecules in the high-risk group. Conclusions: The signature based on 11 DRG-FRG genes stands out as a promising prognostic biomarker for HCC. Beyond its predictive value, it sheds light on the intricate crosstalk between DRG-FRG genes and HCC. Importantly, these findings could pave the way for enhanced prognostic prediction, informed treatment decisions, and the advancement of immunotherapy for HCC patients.

Nanomaterials Regulate Bacterial Quorum Sensing: Applications, Mechanisms, and Optimization Strategies.

Anti-virulence therapy that interferes with bacterial communication, known as "quorum sensing (QS)", is a promising strategy for circumventing bacterial resistance. Using nanomaterials to regulate bacterial QS in anti-virulence therapy has attracted much attention, which is mainly attributed to unique physicochemical properties and excellent designability of nanomaterials. However, bacterial QS is a dynamic and multistep process, and there are significant differences in the specific regulatory mechanisms and related influencing factors of nanomaterials in different steps of the QS process. An in-depth understanding of the specific regulatory mechanisms and related influencing factors of nanomaterials in each step can significantly optimize QS regulatory activity and enhance the development of novel nanomaterials with better comprehensive performance. Therefore, this review focuses on the mechanisms by which nanomaterials regulate bacterial QS in the signal supply (including signal synthesis, secretion, and accumulation) and signal transduction cascade (including signal perception and response) processes. Moreover, based on the two key influencing factors (i.e., the nanomaterial itself and the environment), optimization strategies to enhance the QS regulatory activity are comprehensively summarized. Collectively, applying nanomaterials to regulate bacterial QS is a promising strategy for anti-virulence therapy. This review provides reference and inspiration for further research on the anti-virulence application of nanomaterials.

Graphene-Based Material-Mediated Immunomodulation in Tissue Engineering and Regeneration: Mechanism and Significance.

Tissue engineering and regenerative medicine hold promise for improving or even restoring the function of damaged organs. Graphene-based materials (GBMs) have become a key player in biomaterials applied to tissue engineering and regenerative medicine. A series of cellular and molecular events, which affect the outcome of tissue regeneration, occur after GBMs are implanted into the body. The immunomodulatory function of GBMs is considered to be a key factor influencing tissue regeneration. This review introduces the applications of GBMs in bone, neural, skin, and cardiovascular tissue engineering, emphasizing that the immunomodulatory functions of GBMs significantly improve tissue regeneration. This review focuses on summarizing and discussing the mechanisms by which GBMs mediate the sequential regulation of the innate immune cell inflammatory response. During the process of tissue healing, multiple immune responses, such as the inflammatory response, foreign body reaction, tissue fibrosis, and biodegradation of GBMs, are interrelated and influential. We discuss the regulation of these immune responses by GBMs, as well as the immune cells and related immunomodulatory mechanisms involved. Finally, we summarize the limitations in the immunomodulatory strategies of GBMs and ideas for optimizing GBM applications in tissue engineering. This review demonstrates the significance and related mechanism of the immunomodulatory function of GBM application in tissue engineering; more importantly, it contributes insights into the design of GBMs to enhance wound healing and tissue regeneration in tissue engineering.

MDM2 upregulation induces mitophagy deficiency via Mic60 ubiquitination in fetal microglial inflammation and consequently neuronal DNA damage caused by exposure to ZnO-NPs during pregnancy.

During pregnancy, the human body is quite vulnerable to external stimuli. Zinc oxide nanoparticles (ZnO-NPs) are widely used in daily life, and they enter the human body via environmental or biomedical exposure, thus having potential risks. Although accumulating studies have demonstrated the toxic effects of ZnO-NPs, few studies have addressed the effect of prenatal ZnO-NP exposure on fetal brain tissue development. Here, we systematically studied ZnO-NP-induced fetal brain damage and the underlying mechanism. Using in vivo and in vitro assays, we found that ZnO-NPs could cross the underdeveloped bloodbrain barrier and enter fetal brain tissue, where they could be endocytosed by microglia. ZnO-NP exposure impaired mitochondrial function and induced autophagosome overaccumulation by downregulation of Mic60, thus inducing microglial inflammation. Mechanistically, ZnO-NPs increased Mic60 ubiquitination by activating MDM2, resulting in imbalanced mitochondrial homeostasis. Inhibition of Mic60 ubiquitination by MDM2 silencing significantly attenuated the mitochondrial damage induced by ZnO-NPs, thereby preventing autophagosome overaccumulation and reducing ZnO-NP-mediated inflammation and neuronal DNA damage. Our results demonstrate that ZnO-NPs are likely to disrupt mitochondrial homeostasis, inducing abnormal autophagic flux and microglial inflammation and secondary neuronal damage in the fetus. We hope the information provided in our study will improve the understanding of the effects of prenatal ZnO-NP exposure on fetal brain tissue development and draw more attention to the daily use of and therapeutic exposure to ZnO-NPs among pregnant women.

Tongue-Brain-Transported ZnO Nanoparticles Induce Abnormal Taste Perception.

Nanoparticles (NPs) can be transported to the brain, especially through nerves, because of their small size and high biological activity. Previous studies confirmed that zinc oxide (ZnO) NPs can enter the brain through the tongue-brain pathway, but it is unclear whether they will further affect synaptic transmission and brain perception. In this study, it is found that tongue-brain-transported ZnO NPs can cause a decrease in taste sensitivity and taste aversion learning ability, indicating abnormal taste perception. Moreover, the release of miniature excitatory postsynaptic currents, the frequency of action potential release, and the expression of c-fos are decreased, suggesting that the synaptic transmission is reduced. To further explore the mechanism, protein chip detection of inflammatory factors is carried out and it is found that neuroinflammation occurs. Importantly, it is found that neuroinflammation originated from neurons. The JAK-STAT signaling pathway is activated, which inhibits the Neurexin1-PSD95-Neurologigin1 pathway and c-fos expression. Blocking the activation of the JAK-STAT pathway prevents neuroinflammation and the reduction in Neurexin1-PSD95-Neurologigin1. These results indicate that ZnO NPs can be transported by the tongue-brain pathway and lead to abnormal taste perception by neuroinflammation-induced deficits in synaptic transmission. The study reveals the influence of ZnO NPs on neuronal function and provides a novel mechanism.

Copper oxides activate peroxymonosulfate for degradation of methylene blue via radical and nonradical pathways: surface structure and mechanism.

A one-step hydrothermal method for preparation of copper oxides with different valences using ascorbic acid as a reducing reagent was developed for environmental remediation. The results suggested that the notable degradation performance of CuO0 may be attributable to the abundant active sites, such as Cu or Cu-O, and was not significantly related to the Cu valence state. In contrast to direct degradation of pollutants by traditional superoxide radicals (O2•-), O2•- played an important role in the reduction of high-valence Cu ions (Cu(III)). In addition, a series of radical quenching, electron paramagnetic resonance (EPR), and electrochemical experiments validated the existence of direct electron transfer between methylene blue (MB) and PMS mediated by CuO0 and surface-bound radicals. The results suggested that the CuO0/PMS system may be less susceptible to diverse ions and natural organic matter other than dihydrogen phosphate anions. The mechanism of MB degradation under alkaline conditions was different from that under acidic conditions in that it was not reliant on radicals or charge transfer but direct oxidation by PMS. This study provides new insights into the heterogeneous processes involved in PMS activation by the copper oxides. Furthermore, this paper devotes to providing theoretical basis on pollutant removal via PMS activated by copper oxides and developing low-cost and high-efficiency catalysts.

Stage-specific requirement for METTL3-dependent m6A modification during dental pulp stem cell differentiation.

BACKGROUND: N6-methyladenosine (m6A) is the most prevalent epigenetic modification in eukaryotic messenger RNAs and plays a critical role in cell fate transition. However, it remains to be elucidated how m6A marks functionally impact the transcriptional cascades that orchestrate stem cell differentiation. The present study focuses on the biological function and mechanism of m6A methylation in dental pulp stem cell (DPSC) differentiation. METHODS: m6A RNA immunoprecipitation sequencing was utilized to assess the m6A-mRNA landscape during DPSC differentiation. Ectopic transplantation of DPSCs in immunodeficient mice was conducted to verify the in vitro findings. RNA sequencing and m6A RNA immunoprecipitation sequencing were combined to identify the candidate targets. RNA immunoprecipitation and RNA/protein stability of Noggin (NOG) were evaluated. The alteration in poly(A) tail was measured by 3'-RACE and poly(A) tail length assays. RESULTS: We characterized a dynamic m6A-mRNA landscape during DPSC mineralization with increasing enrichment in the 3' untranslated region (UTR). Methyltransferase-like 3 (METTL3) was identified as the key m6A player, and METTL3 knockdown disrupted functional DPSC differentiation. Moreover, METTL3 overexpression enhanced DPSC mineralization. Increasing m6A deposition in the 3' UTR restricted NOG expression, which is required for DPSC mineralization. This stage-specific m6A methylation and destabilization of NOG was suppressed by METTL3 knockdown only in differentiated DPSCs. Furthermore, METTL3 promotes the degradation of m6A-tagged NOG by shortening the poly(A) tail length in the differentiated stage. CONCLUSIONS: Our results address an essential role of dynamic m6A signaling in the temporal control of DPSC differentiation and provide new insight into epitranscriptomic mechanisms in stem cell-based therapy.

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects.

Biological barriers are essential physiological protective systems and obstacles to drug delivery. Nanoparticles (NPs) can access the paracellular route of biological barriers, either causing adverse health impacts on humans or producing therapeutic opportunities. This Review introduces the structural and functional influences of NPs on the key components that govern the paracellular route, mainly tight junctions, adherens junctions, and cytoskeletons. Furthermore, we evaluate their interaction mechanisms and address the influencing factors that determine the ability of NPs to open the paracellular route, which provides a better knowledge of how NPs can open the paracellular route in a safer and more controllable way. Finally, we summarize limitations in the research models and methodologies of the existing research in the field and provide future research direction. This Review demonstrates the in-depth causes for the reversible opening or destruction of the integrity of barriers generated by NPs; more importantly, it contributes insights into the design of NP-based medications to boost paracellular drug delivery efficiency.

Direct degradation of methylene blue by unactivated peroxymonosulfate: reaction parameters, kinetics, and mechanism.

Advanced oxidation processes (AOPs) are efficient methods for water purification. However, there are few studies on using peroxymonosulfate (PMS) to remove pollutants directly. In this study, about 76% of methylene blue (MB) was removed by PMS directly within 180 min through a non-radical pathway, verified by scavenging tests, electron paramagnetic resonance and kinetic calculations. Additionally, the effects of PMS dosage, MB concentration, temperature, initial pH and competitive anions were determined. High PMS dosage, temperature and pH promoted MB degradation (from 76 to 98%) while MB concentration showed no effect on MB removal. Besides, MB degradation followed pseudo-first-order kinetic with rate constants of 0.0082 to 0.3912 min-1. The second-order rate constant for PMS reaction with MB was 0.08 M-1 s-1 at pH 3-6, but increased dramatically to 4.68 M-1 s-1 at pH 10.50. Chlorine could be catalysed by PMS at high concentration Cl- and degradation efficiency reached 98% within 90 min. High concentration of bicarbonate accelerated MB removal due to the high pH value while humic acid showed a marginal effect on MB degradation. Furthermore, TOC removal rate of MB in the presence of chloride reached 45%, whereas PMS alone caused almost no mineralisation. This study provides new insights into pollutant removal and an additional strategy for water purification.

Long non-coding RNA LINC01793 as a potential diagnostic biomarker of hepatitis B virus-related hepatocellular carcinoma.

BACKGROUND: There is growing evidence that long non-coding RNAs (lncRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) and may serve as diagnostic markers. This study investigates the diagnostic efficiency of the long intergenic non-protein-coding RNA 1793 (LINC01793) in hepatitis B virus (HBV)-related HCC. METHODS: Bioinformatics methods were used to screen the aberrantly expressed lncRNAs in HCC tissues based on The Cancer Genome Atlas (TCGA). Quantitative reverse transcription polymerase chain reaction was performed to assess the expression of the candidate lncRNAs in tissues, cells and whole blood samples of patients with HBV-related HCC, liver cirrhosis (LC), chronic hepatitis (CHB), and healthy controls. Then, the correlations between LINC01793 and clinical characteristics were analyzed. Finally, the diagnostic value of LINC01793 was explored based on the receiver operating characteristic curve. RESULTS: LINC01793 was remarkably upregulated in the HCC tissues and cells. It was highly expressed in the whole blood of the HBV-related HCC patients, unlike in that of the healthy controls and of the CHB and LC patients. Subsequent analysis revealed that high LINC01793 was related to the Barcelona Clinic Liver Cancer (P = 0.007), tumor invasion (P = 0.042), the number of tumors (P = 0.031) and serum level of alanine aminotransferase(p = 0.022). The areas under the curve of LINC01793, for distinguishing HCC from healthy controls, CHB and LC patients, were 0.824, 0.767 and 0.756, respectively. In addition, the combination of LINC01793 with alpha fetoprotein (AFP) had a stronger diagnostic value than LINC01793 or AFP alone in AFP-negative HCC patients. CONCLUSION: High expression of LINC01793 is correlated with adverse clinical characteristics and can serve as a non-invasive biomarker of HCC.

Improvement of synaptic plasticity by nanoparticles and the related mechanisms: Applications and prospects.

Synaptic plasticity is an important basis of learning and memory and participates in brain network remodelling after different types of brain injury (such as that caused by neurodegenerative diseases, cerebral ischaemic injury, posttraumatic stress disorder (PTSD), and psychiatric disorders). Therefore, improving synaptic plasticity is particularly important for the treatment of nervous system-related diseases. With the rapid development of nanotechnology, increasing evidence has shown that nanoparticles (NPs) can cross the blood-brain barrier (BBB) in different ways, directly or indirectly act on nerve cells, regulate synaptic plasticity, and ultimately improve nerve function. Therefore, to better elucidate the effect of NPs on synaptic plasticity, we review evidence showing that NPs can improve synaptic plasticity by regulating different influencing factors, such as neurotransmitters, receptors, presynaptic membrane proteins and postsynaptic membrane proteins, and further discuss the possible mechanism by which NPs improve synaptic plasticity. We conclude that NPs can improve synaptic plasticity and restore the function of damaged nerves by inhibiting neuroinflammation and oxidative stress, inducing autophagy, and regulating ion channels on the cell membrane. By reviewing the mechanism by which NPs regulate synaptic plasticity and the applications of NPs for the treatment of neurological diseases, we also propose directions for future research in this field and provide an important reference for follow-up research.

Diagnostic value of long noncoding RNA LINC01485 in patients with colorectal cancer.

BACKGROUND: Long noncoding RNAs (lncRNAs) were considered as transcription noise without biological functions. However, accumulated evidence shows that lncRNAs are expressed heterogeneously in tumor tissues. This study aims to identify the specific expression of lncRNAs in colorectal cancer patients and to perform verification analysis. METHODS: The differentially expressed lncRNAs and mRNAs in colorectal cancer and normal tissues were screened by bioinformatics methods. Subsequently, the qRT-PCR method was used to verify the expression of differential lncRNAs in tumor tissues and blood samples. Concurrently ROC curves were used to analyze the diagnostic efficacy of lncRNAs. Moreover, the correlation between lncRNAs and clinicopathological features was also analyzed. Finally, functional annotation analysis was performed for lncRNAs. RESULTS: Eleven lncRNAs differentially expressed in colorectal cancer tissues and normal tissues were screened. In the validation tissue sample set, FOXD3-AS1 was down-regulated in colorectal cancer tissues (P < 0.001), while LINC01485 was up-regulated in colorectal cancer tissues compared with the adjacent tissues (P < 0.05). In a further verification of the whole blood sample set, LINC01485 showed high sensitivity and specificity (sensitivity = 98.33%, specificity = 84.00%) in differentiating colorectal cancer patients from healthy controls (P < 0.001). Simultaneously, there was no difference in the expression of LINC01485 in other gastrointestinal tumors (hepatocellular carcinoma, esophageal cancer, gastric cancer, and pancreatic cancer) and healthy controls. LINC01485 is significantly related to the clinical staging, lymph node metastasis, and distant metastasis of colorectal cancer. CONCLUSIONS: The expression, diagnostic efficiency, and functional analysis of the lncRNA file of colorectal cancer reveals the important role of LINC01485 in colorectal cancer and provides an important clinical reference value for the early diagnosis and targeted therapy of colorectal cancer.

ß -Glucan Improves Protective Qi Status in Adults with Protective Qi Deficiency-A Randomized, Placebo-Controlled, and Double-Blinded Trial.

OBJECTIVE: To test the hypothesis that ß -glucan enhances protective qi (PQi), an important Chinese medicine (CM) concept which stipulates that a protective force circulates throughout the body surface and works as the first line of defense against "external pernicious influences". METHODS: A total of 138 participants with PQi deficiency (PQD) were randomized to receive ß -glucan (200 mg daily) or placebo for 12 weeks. Participants' PQi status was assessed every 2 weeks via conventional diagnosis and a standardized protocol from which a PQD severity and risk score was derived. Indices of participants' immune and general health status were also monitored, including upper respiratory tract infection (URTI), saliva secretory IgA (sIgA), and self-reported measures of physical and mental health (PROMIS). RESULTS: PQi status was not significantly different between the ß -glucan and placebo treatment groups at baseline but improved significantly in the ß -glucan (vs. placebo) group in a time-dependent manner. The intergroup differences [95% confidence interval (CI)] in severity score (scale: 1-5), risk score (scale: 0-1), and proportion of PQD participants (%) at finish line was 0.49 (0.35-0.62), 0.48 (0.35-0.61), and 0.36 (0.25-0.47), respectively. Additionally, ß -glucan improved URTI symptom (scale: 1-9) and PROMIS physical (scale: 16.2-67.7) and mental (scale: 21.2-67.6) scores by a magnitude (95% CI) of 1.0 (0.21-1.86), 5.7 (2.33-9.07), and 3.0 (20.37-6.37), respectively, over placebo. CONCLUSIONS: ß -glucan ameliorates PQi in PQD individuals. By using stringent evidence-based methodologies, our study demonstrated that Western medicine-derived remedies, such as ß -glucan, can be employed to advance CM therapeutics. (ClinicalTrial.Gov registry: NCT03782974).

Electrochemically derived nanographene oxide activates endothelial tip cells and promotes angiogenesis by binding endogenous lysophosphatidic acid.

Graphene oxide (GO) exhibits good mechanical and physicochemical characteristics and has extensive application prospects in bone tissue engineering. However, its effect on angiogenesis is unclear, and its potential toxic effects are heavily disputed. Herein, we found that nanographene oxide (NGO) synthesized by one-step water electrolytic oxidation is smaller and shows superior biocompatibility. Moreover, NGO significantly enhanced angiogenesis in calvarial bone defect areas in vivo, providing a good microenvironment for bone regeneration. Endothelial tip cell differentiation is an important step in the initiation of angiogenesis. We verified that NGO activates endothelial tip cells by coupling with lysophosphatidic acid (LPA) in serum via strong hydrogen bonding interactions, which has not been reported. In addition, the mechanism by which NGO promotes angiogenesis was systematically studied. NGO-coupled LPA activates LPAR6 and facilitates the formation of migratory tip cells via Hippo/Yes-associated protein (YAP) independent of reactive oxygen species (ROS) stimulation or additional complex modifications. These results provide an effective strategy for the application of electrochemically derived NGO and more insight into NGO-mediated angiogenesis.

GO-based antibacterial composites: Application and design strategies.

Graphene oxide (GO), for its unique structure with high biocompatibility and designability, is widely used in the antibacterial field. Various strategies have been designed to fabricate GO-based composites with antibacterial properties. This review summarized these strategies, divided them into three types and interpreted their antibacterial mechanisms: (i) "GO*/non-GO" type in which GO acts as the single antibacterial core, (ii) "GO*/non-GO*" type in which GO and non-GO components function synergistically as dual antibacterial cores, (iii) "GO/non-GO*" type in which non-GO acts as the single antibacterial core, while GO component plays a supportive, not a dominant role in antibiosis. Besides, the fields suiting their applications and factors influencing their antibacterial properties were analyzed. Finally, the limitations and prospects in the current researches were discussed. In summary, GO-based composites have revolutionized antibacterial strategies. This review may serve as a reference to inspire further research on GO-based antibacterial composites.

Graphene-based nanomaterials for breast cancer treatment: promising therapeutic strategies.

Breast cancer is the most common malignancy in women, and its incidence increases annually. Traditional therapies have several side effects, leading to the urgent need to explore new smart drug-delivery systems and find new therapeutic strategies. Graphene-based nanomaterials (GBNs) are potential drug carriers due to their target selectivity, easy functionalization, chemosensitization and high drug-loading capacity. Previous studies have revealed that GBNs play an important role in fighting breast cancer. Here, we have summarized the superior properties of GBNs and modifications to shape GBNs for improved function. Then, we focus on the applications of GBNs in breast cancer treatment, including drug delivery, gene therapy, phototherapy, and magnetothermal therapy (MTT), and as a platform to combine multiple therapies. Their advantages in enhancing therapeutic effects, reducing the toxicity of chemotherapeutic drugs, overcoming multidrug resistance (MDR) and inhibiting tumor metastasis are highlighted. This review aims to help evaluate GBNs as therapeutic strategies and provide additional novel ideas for their application in breast cancer therapy.

Understanding the interactions between inorganic-based nanomaterials and biological membranes.

The interactions between inorganic-based nanomaterials (NMs) and biological membranes are among the most important phenomena for developing NM-based therapeutics and resolving nanotoxicology. Herein, we introduce the structural and functional effects of inorganic-based NMs on biological membranes, mainly the plasma membrane and the endomembrane system, with an emphasis on the interface, which involves highly complex networks between NMs and biomolecules (such as membrane proteins and lipids). Significant efforts have been devoted to categorizing and analyzing the interaction mechanisms in terms of the physicochemical characteristics and biological effects of NMs, which can directly or indirectly influence the effects of NMs on membranes. Importantly, we summarize that the biological membranes act as platforms and thereby mediate NMs-immune system contacts. In this overview, the existing challenges and potential applications in the areas are addressed. A strong understanding of the discussed concepts will promote therapeutic NM designs for drug delivery systems by leveraging the NMs-membrane interactions and their functions.

Response of the microbial community to phosphate-solubilizing bacterial inoculants on Ulmus chenmoui Cheng in Eastern China.

Phosphate-solubilizing bacteria (PSB) have beneficial effects on plant health and soil composition. To date, studies of PSB in soil have largely been performed under field or greenhouse conditions. However, less is known about the impact of introducing indigenous PSB in the field, including their effects on the local microbial community. In this study, we conducted greenhouse and field experiments to explore the effects of the addition of indigenous PSB on the growth of Chenmou elm (Ulmus chenmoui) and on the diversity and composition of the bacterial community in the soil. We obtained four bacterial isolates with the highest phosphate-solubilizing activity: UC_1 (Pseudomonas sp.), UC_M (Klebsiella sp.), UC_J (Burkholderia sp.), and UC_3 (Chryseobacterium sp.). Sequencing on the Illumina MiSeq platform showed that the inoculated PSB did not become the dominant strains in the U. chenmoui rhizosphere. However, the soil bacterial community structure was altered by the addition of these PSB. The relative abundance of Chloroflexi decreased significantly in response to PSB application in all treatment groups, whereas the populations of several bacteria, including Proteobacteria and Bacteroidetes, increased. Network analysis indicated that Chloroflexi was the most strongly negatively correlated with Proteobacteria, whereas Proteobacteria was strongly positively correlated with Bacteroidetes. Our findings indicate that inoculation with PSB (UC_1, UC_M, UC_J, and UC_3) can improve the growth of U. chenmoui and regulate its rhizosphere microbial community. Therefore, inoculation with these bacterial strains could promote the efficient cultivation and production of high-quality plant materials.

Proof-of-Concept and Feasibility Study to Evaluate the Effect of ß-Glucan on Protective Qi Deficiency in Adults.

OBJECTIVE: To preliminarily explore the potential effect of ß-glucan on Chinese medicine (CM) concept protective qi deficiency (PQD), and the methodology for future definitive studies. METHODS: To have a standardized assessment of PQD, a list of 13 potentially PQD-relevant parameters were firstly created, each with defined quantitative or categorial scales. Using the data from 37 participants with (21 cases) or without (16 cases) PQD, multivariate logistic modeling was conducted to create a preliminary diagnostic PQD risk score. Subsequently, 21 participants diagnosed with PQD were treated with ß-glucan in a dose of 200 mg/day for 8 weeks. Data were collected for trial acceptability measures (rate of recruitment, withdrawal, and compliance), and the participants were assessed for PQD status at baseline and every 2 weeks thereafter. RESULTS: The preliminary logistic model consisted of 3 parameters (low voice and apathy, aversion to wind and cold, and Cun pulse). The resulting risk score demonstrated a degree of PQD-predicting accuracy that, as evaluated by statistical (discrimination and classification) methods, was higher than those obtained from any of the individual candidate parameters. The 21 PQD participants treated with ß-glucan demonstrated good receptibility and a time-dependent improvement in PQD status as evidenced by the decrease of PQD participant to 9.5% at the end of study. CONCLUSIONS: This study demonstrated the effect of proof-of-concept of ß-glucan on improving PQD and the proof-of-concept of a multivariate-model-derived diagnostic PQD risk score. It also indicated feasibility for future definitive studies. Studies like this embody an innovative approach that uses therapies derived from the mainstream biomedicine to enrich therapeutics guided by CM principle. (Trial registration No. NCT03829228).