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Aim The aims of this study were to examine the prevalence of adverse childhood experiences (ACEs) among health science students in China; associations between the number of ACE exposures and severity of depressive and anxiety symptoms; and the extent to which resilience moderates the effect of ACEs on mental health outcomes. Design This descriptive, cross-sectional study was conducted May-August 2020. Methods Five hundred and sixty-six health science students (18-38 years) from China completed online surveys measuring ACEs using the Simplified Chinese version of the ACE-International Questionnaire, depressive and anxiety symptoms and resilience. Descriptive statistical analysis, ANOVA with Tukey HSD post hoc tests and multiple regression analysis were performed using SPSS 27. Results 88.5% of participants reported at least one ACE; 42.6% reported four or more ACEs. Higher number of ACEs was associated with more symptoms of depression and anxiety. Four or more ACEs were associated with significantly worse mental health outcomes than those with no ACEs and those with one to three ACEs. Greater resilience significantly attenuated the effects of ACEs on mental health symptoms. Conclusions ACEs are highly prevalent among Chinese health science students but their impact on mental health can be buffered by higher levels of resilience. Impact Screening for ACEs and strength-based, trauma-informed interventions on fostering resilience is needed to promote mental health among Chinese young adults.

Background We explored whether stem cell therapy was effective for animal models and patients with Crohn’s disease (CD). Methods We searched five online databases. The relative outcomes were analyzed with the aid of GetData Graph Digitizer 2.26 and Stata 16.0 software. The SYRCLE risk of bias tool and the MINORS tool were used to assess study quality. Results We evaluated 46 studies including 28 animal works (n = 567) and 18 human trials (n = 360). In the animal studies, the disease activity index dramatically decreased in the mesenchymal stem cell (MSC) treatment groups compared to the control group. Rats and mice receiving MSCs exhibited longer colons [mice: standardized mean difference (SMD) 2.84, P = 0.000; rats: SMD 1.44, P = 0.029], lower histopathological scores (mice: SMD − 4.58, p = 0.000; rats: SMD − 1.41, P = 0.000) and lower myeloperoxidase levels (SMD − 6.22, P = 0.000). In clinical trials, stem cell transplantation reduced the CD activity index (SMD − 2.10, P = 0.000), the CD endoscopic index of severity (SMD − 3.40, P = 0.000) and simplified endoscopy score for CD (SMD − 1.71, P = 0.000) and improved the inflammatory bowel disease questionnaire score (SMD 1.33, P = 0.305) compared to control values. CD patients maintained high remission rates for 3–24 months after transplantation. Conclusions Stem cell transplantation is a valuable supplementary therapy for CD.

Liver injury has caused significant illness in humans worldwide. The dynamics of intestinal bacterial communities associated with natural recovery and therapy for CCl4-treated liver injury remain poorly understood. This study was designed to determine the recovery dynamics of intestinal bacterial communities in CCl4-treated mice with or without mesenchymal stem cell transplantation (i.e., MSC and CCl4 groups) at 48 h, 1 week (w), and 2 w. MSCs significantly improved the histopathology, survival rate, and intestinal structural integrity in the treated mice. The gut bacterial communities were determined with significant changes in both the MSC and CCl4 groups over time, with the greatest difference between the MSC and CCl4 groups at 48 h. The liver injury dysbiosis ratio experienced a decrease in the MSC groups and a rise in the CCl4 groups over time, suggesting the mice in the MSC group at 48 h and the CCl4 group at two weeks were at the least gut microbial dysbiosis status among the corresponding cohorts. Multiple OTUs and functional categories were associated with each of the bacterial communities in the MSC and CCl4 groups over time. Among these gut phylotypes, OTU1352_S24-7 was determined as the vital member in MSC-treated mice at 48 h, while OTU453_S24-7, OTU1213_Ruminococcaceae, and OTU841_Ruminococcus were determined as the vital phylotypes in CCl4-treated mice at two weeks. The relevant findings could assist the diagnosis of the microbial dysbiosis status of intestinal bacterial communities in the CCl4-treated cohorts with or without MSC transplantation.

Diabetes mellitus (DM) is a chronic metabolic disease with high morbidity and mortality. Recently, stem cell-based therapy for DM has shown considerable promise. Here, we undertook a systematic review and meta-analysis of published clinical studies to evaluate the efficacy and safety of stem cell therapy for both type 1 DM (T1DM) and type 2 DM (T2DM). The PubMed, Cochrane Central Register of Controlled Trials, EMBASE, and ClinicalTrials.gov databases were searched up to November 2018. We employed a fixed-effect model using 95% confidence intervals (CIs) when no statistically significant heterogeneity existed. Otherwise, a random-effects statistical model was used. Twenty-one studies met our inclusion criteria: ten T1DM studies including 226 patients and eleven T2DM studies including 386 patients. Stem cell therapy improved C-peptide levels (mean difference (MD), 0.41; 95% CI, 0.06 to 0.76) and glycosylated hemoglobin (HbA1c; MD, -3.46; 95% CI, -6.01 to -0.91) for T1DM patients. For T2DM patients, stem cell therapy improved C-peptide levels (MD, 0.33; 95% CI, 0.07 to 0.59), HbA1c (MD, -0.87; 95% CI, -1.37 to -0.37) and insulin requirements (MD, -35.76; 95% CI, -40.47 to -31.04). However, there was no significant change in fasting plasma glucose levels (MD, -0.52; 95% CI, -1.38 to 0.34). Subgroup analyses showed significant HbA1c and C-peptide improvements in patients with T1DM treated with bone marrow hematopoietic stem cells (BM-HSCs), while there was no significant change in the mesenchymal stem cell (MSC) group. In T2DM, HbA1c and insulin requirements decreased significantly after MSC transplantation, and insulin requirements and C-peptide levels were significantly improved after bone marrow mononuclear cell (BM-MNC) treatment. Stem cell therapy is a relatively safe and effective method for selected individuals with DM. The data showed that BM-HSCs are superior to MSCs in the treatment of T1DM. In T2DM, MSC and BM-MNC transplantation showed favorable therapeutic effects.

The placenta and umbilical cord are pre-eminent candidate sources of mesenchymal stem cells (MSCs). However, placenta-derived MSCs (P-MSCs) showed greater proliferation capacity than umbilical cord-derived MSCs (UC-MSCs) in our study. We investigated the drivers of this proliferation difference and elucidated the mechanisms of proliferation regulation. Proteomic profiling and Gene Ontology (GO) functional enrichment were conducted to identify candidate proteins that may influence proliferation. Using lentiviral or small interfering RNA infection, we established overexpression and knockdown models and observed changes in cell proliferation to examine whether a relationship exists between the candidate proteins and proliferation capacity. Real-time quantitative polymerase chain reaction, western blot analysis, and immunofluorescence assays were conducted to elucidate the mechanisms underlying proliferation. Six candidate proteins were selected based on the results of proteomic profiling and GO functional enrichment. Through further validation, yes-associated protein 1 (YAP1) and β-catenin were confirmed to affect MSCs proliferation rates. YAP1 and β-catenin showed increased nuclear colocalization during cell expansion. YAP1 overexpression significantly enhanced proliferation capacity and upregulated the expression of both β-catenin and the transcriptional targets of Wnt signaling, CCND1, and c-MYC, whereas silencing β-catenin attenuated this influence. We found that YAP1 directly interacts with β-catenin in the nucleus to form a transcriptional YAP/β-catenin/TCF4 complex. Our study revealed that YAP1 and β-catenin caused the different proliferation capacities of P-MSCs and UC-MSCs. Mechanism analysis showed that YAP1 stabilized the nuclear β-catenin protein, and also triggered the Wnt/β-catenin pathway, promoting proliferation.

Background and Aims: Viral hepatitis are one of the main causes of liver cirrhosis. The treatment of portal hypertension caused by liver cirrhosis is difficult and diverse, and the therapeutic effect is unknown. Bayesian network meta-analysis was performed to compare the efficacy and safety of treatments for patients with portal hypertension and cirrhosis, including a transjugular intrahepatic portosystemic shunt (TIPS), endoscopic therapy, surgical therapy and medications.Methods: Eligible articles were searched for in PubMed, Embase, Cochrane Library and Web of Science databases from their inception until June 2020. Using the “gemtc-0.8.4” package in R v.3.6.3 software and the Just Another Gibbs Sampler v.4.2.0 program, network meta-analysis was performed using a random effects model within a Bayesian framework. The odds ratios for all-cause rebleeding, bleeding-related mortality, overall survival (OS), treatment failure and hepatic encephalopathy were determined within the Bayesian framework.Results: Forty randomized controlled trials were identified, including 4,006 adult patients and nine treatment strategies. Our results showed that distal splenorenal shunt and TIPS provided the best control of hemorrhage. Endoscopic variceal ligation with medication resulted in the highest OS rate. Medication alone resulted in poor OS and treatment failure.Conclusions: We performed a systematic comparison of diverse treatments for cirrhotic patients with portal hypertension. Our meta-analysis indicated that a TIPS and distal splenorenal shunt resulted in lower rates of rebleeding than did other therapies. Furthermore, drugs are more suitable for combination therapy than monotherapy.

Background: Organoid culture enables disease modeling and drug screening in vitro. Organoids are from organs (e.g., brain, small intestine, kidney, lung, and liver). To facilitate the establishment of liver and small-intestinal organoids, we developed a protocol for collecting cholangiocytes and crypts and culturing organoids.Methods: Cholangiocytes were collected from intrahepatic bile ducts, gallbladder, and crypts from the small intestine using gravity settling and multi-step centrifugation methods, and embedded in Matrigel to grow into three-dimensional spheroids in suitable culture medium. Passaging, cryopreservation, and thawing were performed to assess organoid cell stability. RNA and DNA extraction, as well as immunostaining procedure were optimized. For preclinical modeling, the growth rate of cholangiocyte organoids (cho-orgs) was harmonized.Results: Large amount of Cholangiocytes and small intestine crypts were collected. Cholangiocytes developed into cyst-like structures after 3–4 days in Matrigel. After culture for 1–2 weeks, small-intestinal organoids developed buds and formed a mature structure. Cho-orgs from intrahepatic bile ducts grew more slowly but were longer lasting, expressed the cholangiocyte markers Krt19 and Krt7, and recapitulated the in vivo tissue organization.Conclusions: The protocol takes 2–4 weeks to establish a stable organoid growth system. Organoids could be stably passaged, cryopreserved, and recovered. The organoids retained tissue characteristics, including marker expression.

Background: Ferroptosis, a newly recognized form of regulated cell death, was recently identified as a novel therapeutic target in tissue injury. Various studies have shown that administration of mesenchymal stem cells (MSC) is a promising therapeutic approach to repair liver injury. However, the role of ferroptosis in acute liver injury (ALI) and MSC-based therapy is unknown. Results: Here we found that CCl4 induced elevated lipid reactive oxygen species (lipid-ROS) and mRNA levels of putative molecular markers of ferroptosis such as Ptgs2 and LOX genes. CCl4 also downregulated the xCT protein levels resulting in the accumulation of lipid peroxidation and ferroptosis. MSC transplantation largely abolished CCl4-induced ferroptosis. Furthermore, the protective effects of MSC against ferroptosis were closely correlated with exosome-mediated stabilization of xCT. Administration of MSC-Exo restored the xCT protein level, decreased the elevated lipid-ROS level and Ptgs2 and LOX mRNA levels, and promoted liver restoration by inhibiting ferroptosis. Interestingly, in ALI mouse livers after MSC-Exo treatment, exosome-induced recovery of xCT protein was accompanied by upregulation of CD44 and OTUB1. The level of ubiquitinated xCT upregulated by CCl4 was significantly downregulated by OTUB1-mediated deubiquitination, and strong interactions of xCT with OTUB1 and CD44 proteins were detected. Conclusions: Taken together, our data indicate that MSC-Exo has a protective role against ferroptosis by maintaining xCT function. This provides a novel therapeutic strategy for ferroptosis-induced ALI.

Diabetic retinopathy (DR) is a common condition of diabetes, and approaches to detecting early DR using the unique characteristics of the retinal pigment epithelium-Bruch’s membrane complex (RBC) have increasingly attracted attention. A diabetic model was established in Sprague-Dawley rats via streptozocin (STZ) injection for 1 (DM1) and 6 months (DM6), confirmed by weekly blood glucose measurement. Serum and retinal tissue-based advanced glycation endproducts (AGE) levels significantly elevated in diabetic rats, and RBC was evaluated by transmission electron microscopy and Raman spectroscopy. The results showed that whole Raman spectra and all marked band intensities could respectively achieve almost equal and accurate discrimination of all animal groups, along with the determination of important molecules from the band data. Further quantitative analyses indicated series of metabolic disturbance due to hyperglycemia were involved while the body self-regulation mechanism still played a role with different effects during the disease progression. Given this, Raman spectroscopy can reliably distinguish the early characterization of DR in addition to providing intrinsic key molecules that is sensitive to identify the early disease progression.

Systemic inflammatory processes, including alveolar injury, cytokine induction, and neutrophil accumulation, play key roles in the pathophysiology of acute lung injury (ALI). The immunomodulatory effects of mesenchymal stem cells (MSCs) can contribute to the treatment of inflammatory disorders. In previous studies, the focus was on innate immune cells and the effects of MSCs on ALI through CD8+ T cells remain unclear. In the present study, lipopolysaccharide (LPS) was used to induce ALI in mice. ALI mice were treated with MSCs via intratracheal instillation. Survival rate, histopathological changes, protein levels, total cell count, cytokine levels, and chemokine levels in alveolar lavage fluid were used to determine the efficacy of MSCs. Mass cytometry and single-cell RNA sequencing (scRNA-seq) were used to characterize the CD8+ T cells in the lungs. Ly6C− CD8+ T cells are prevalent in normal mice, whereas a specialized effector phenotype expressing a high level of Ly6C is predominant in advanced disease. MSCs significantly mitigated ALI and improved survival. MSCs decreased the infiltration of CD8+ T cells, especially Ly6C+ CD8+ T cells into the lungs. Mass cytometry revealed that CD8+ T cells expressing high Ly6C and CXCR3 levels caused tissue damage in the lungs of ALI mice, which was alleviated by MSCs. The scRNA-seq showed that Ly6C+ CD8+ T cells exhibited a more activated phenotype and decreased expression of proinflammatory factors that were enriched the most in immune chemotaxis after treatment with MSCs. We showed that CD8+ T cells play an important role in MSC-mediated ALI remission, and both infiltration quantity and proinflammatory function were inhibited by MSCs, indicating a potential mechanism for therapeutic intervention.

Hepatorenal syndrome (HRS) is a severe complication of decompensated cirrhosis with high mortality. However, few prognostic factors have been identified and studies are urgently needed to facilitate precise treatment.Patients with decompensated cirrhosis and acute kidney injury were enrolled from four general hospitals between January 2010 and March 2020. Demographic and laboratory data were compared between surviving and non-surviving patients and also among different levels of HRS severity. COX regression analysis was performed to determine the effect of mean corpuscular hemoglobin concentration (MCHC) on survival of patients with HRS.Out of a total of 1287 patients enrolled, 325 patients were analyzed. MCHC was significantly higher in non-survivors than in survivors, and in patients with more serious disease, defined as failure of organ systems. The hazard ratio (HR) of mortality was 1.17, 1.18 and 1.11, when adjusted by the crude model, model 1 and model 2, respectively. When MCHC was converted to a categorical variable based on the quartile of MCHC, the HR for the highest quartile of MCHC was 2.11 (95% CI: 1.45-3.06, P0.05) compared to the lowest quartile of MCHC in the crude model, and when adjusted for age and sex (model 1), the HR was 2.20 (95% CI: 1.52-3.20, P0.05). In model 2, which was adjusted for complex characteristics, the HR was 1.77 (95% CI: 1.17-2.68, P0.05). The results of Kaplan-Meier curves were consistent with those from Cox regression analysis.Higher MCHC was associated with worse prognosis in HRS.

Background Immune system disorders play important roles in acute lung injury (ALI), and mesenchymal stem cell (MSC) treatment can reduce inflammation during ALI. In this study, we compared the changes in lung B cells during MSC treatment. Methods We investigated the effects of MSCs on lung B cells in a mouse model of lipopolysaccharide (LPS)-induced ALI. MSCs were administered intratracheally 4 h after LPS. As vehicle-treated controls, mice were treated with phosphate-buffered saline (PBS) containing 2% C57BL/6 (PBS group). Histopathological changes, survival rate, inflammatory factor levels, and the number of neutrophils in bronchoalveolar lavage fluid (BALF) were determined. Single-cell RNA sequencing (scRNA-Seq) analysis was performed to evaluate the transcriptional changes in lung B cells between the PBS, LPS, and LPS/MSC groups on days 3 and 7. Results MSC treatment ameliorated LPS-induced ALI, as indicated by the reductions in mortality, the levels of chemokines and cytokines in BALF, and the severity of lung tissue histopathology in ALI mice. Lung B cells in the PBS group remained undifferentiated and had an inhibitory phenotype. Based on our scRNA-Seq results, the differentially expressed genes (DEGs) in lung B cells in both the PBS group and LPS group were involved in chemotaxis processes and some proinflammatory pathways. MSC treatment inhibited the expression of chemokine genes that were upregulated by LPS and were related to the recruitment of neutrophils into lung tissues. Immunoglobulin-related gene expression was decreased in lung B cells of mice treated with LPS/MSC for 7 days. The DEGs regulated by MSCs were enriched in biological processes, including humoral immune response and apoptotic signaling. Conclusions Lung B cells played an important role in the effects of treatment of ALI with MSCs. These observations provide new insights into the mechanisms underlying the effects of MSC treatment for ALI.

The aim of the study was to identify the characteristics and outcomes in acute-on-chronic liver failure (ACLF) patients with or without cirrhosis using two criteria. Patients with acute deterioration of chronic hepatic disease or acute decompensation of cirrhosis were included retrospectively from April 10, 2016 to April 10, 2019. European Association for the Study of the Liver-chronic liver failure (EASL-CLIF) criterion except for consideration of cirrhosis and Chinese Group on the Study of Severe Hepatitis B (COSSH) criterion were used. Clinical features, laboratory data and survival curves were compared between the ACLF patients with and without cirrhosis. A total of 799 patients were included. Among them, 328 had COSSH and EASL ACLF, 197 had COSSH alone, and 104 had EASL alone. There were 11.6% more ACLF with COSSH criterion. Furthermore, EASL ACLF patients with non-cirrhosis vs. cirrhosis had different laboratory characteristics: ALT (423 vs. 154, p p p p p p = 0.398) and 90-day (p = 0.376) survival curves. However, 90-day (p = 0.030) survival curve was different between non-cirrhosis and cirrhosis in COSSH ACLF patients. COSSH ACLF score (auROC = 0.778 or 0.792, 95%CI 0.706–0.839 or 0.721–0.851) displayed the better prognostic ability for EASL ACLF patients with non-cirrhosis, but CLIF-C ACLF score (auROC = 0.757 or 0.796, 95%CI 0.701–0.807 or 0.743–0.843) still was the best prognostic scoring system in EASL ACLF patients with cirrhosis. In conclusions, EASL definition exhibited better performance on homogeneous identification of ACLF regardless of cirrhosis or non-cirrhosis. And COSSH ACLF score displayed the better prognostic ability for EASL ACLF patients without cirrhosis.

To disclose how phosphorus deficiency influence phytoremediation of Cd contamination using poplars, root architecture, Cd absorption, Cd translocation and antioxidant defense in poplar roots were investigated using a clone of Populus × euramericana. Root growth was unaltered by Cd exposure regardless of P conditions, while the degree of root proliferation upon P deficiency was changed by high level of Cd exposure. The concentration and content of Cd accumulation in roots were increased by P deficiency. This can be partially explained by the increased expression of genes encoding PM H + -ATPase under the combined conditions of P deficiency and high Cd exposure, which enhanced Cd2+-H+ exchanges and led to an increment of Cd uptake under P deficiency. Despite of the increasing Cd accumulation in roots, the translocation of Cd from roots to aerial tissues sharply decreased upon P deficiency. The relative expression of genes responsible for Cd translocation (HMA4) decreased upon P deficiency and thus inhibited Cd translocation via xylem. GR activity was decreased by P deficiency, which can inhibit the form of GSH and GSH–Cd complexes and decrease Cd translocation via GSH–Cd complexes. The transportation of PC–Cd complexes into vacuole decreased under P deficiency as a result of the low expression of PCS and ABCC1, and thus suppressed Cd tolerance and Cd detoxification in roots. Moreover, P deficiency decreased the levels of antioxidase (GR and CAT) and phytohormones including JA, ABA and GA3, which synchronously reduced antioxidant capacity in roots.

An emulsion interface materialization method was used to obtain amphiphilic silica Janus nanoparticles. Reducing the photosynthesis of aquatic organisms after water pollution. PW12O403− was introduced onto Janus particles by ion exchange, and an amphiphilic particle emulsion catalyst (PWO-J) was prepared. Hydrogen peroxide was used as the oxygen source, and the amphiphilicty of the catalyst was used to assemble the catalyst at the Pickering emulsion interface. The PWO-J catalyst was found to exhibit very high catalytic activity toward the oxidation of oleic acid in water-in-oil systems. The results showed that PWO-J catalysis of oxidation had similar results as CTAB and phosphotungstic acid (control system) under the same conditions. The azelaic acid recovery rate was 86.7%, and PWO-J could be reused 4 times. A reaction mechanism was proposed, and the constructed model was used to calculate a reaction rate constant of 15.32 × 10−5L•mol−1•s−1 for the PWO-J system. The PWO-J system had a lower activation energy than the control system, showing that the catalytic oxidation of oleic acid into azelaic acid was more likely to occur in the PWO-J system.

The soils in mining lands with cadmium (Cd) contamination usually are deficient in nutrients. Disclosing how P nutrition and N:P stoichiometric ratio influences Cd accumulation and stress tolerance in stems of Populus spp. will facilitate the phytoremediation of mining sites polluted by Cd. In this study, investigations at the anatomical and physiological levels were conducted using a clone of Populus × euramericana. Both phosphorus deficiency and cadmium exposure inhibited xylem development via reducing cell layers in the xylem. Under P-sufficient condition, appropriate P status and balanced N:P ratio in stem promoted xylem development under Cd exposure via stimulating cell division, which enhanced Cd accumulation in stems. Cd accumulation in cell walls of collenchyma tissues of the stem was enhanced by P application due to increased polysaccharide production and cell wall affinity for Cd. The low P concentrations (0.3–0.4 mg g−1) and imbalanced N:P ratio under P deficiency inhibited the production of APX and ascorbate–GSH cycle, which increased oxidative stress and lipid peroxidation as indicated by high MDA concentration in stem. Under P-sufficient condition, the interactions between phytohormones and antioxidants play crucial roles in the process of antioxidant defense under Cd exposure. In conclusions, appropriate P addition and balanced N:P ratio enhanced secondary xylem development and promoted cadmium accumulation and stress tolerance in Populus stems, which can benefit the phytoextraction of Cd from Cd-contaminated soil.

Background The efficacy of mesenchymal stem cell (MSC)-based therapy for acute liver injury (ALI) involves coordination with the hepatic immune system, a complex and coordinated network of immune-cell interactions. However, studies of the immunomodulatory effects of MSCs have focused on a limited number of cell subsets rather than a systematic assessment. Methods Carbon tetrachloride (CCl4) was used to induce ALI in mice. To determine the efficacy of MSCs, ALI mice were injected with MSCs via the tail vein, and histopathological changes, survival rate, and the serum levels of liver enzymes were determined. To assess the immune response induced by MSCs, a mass cytometry panel of 43 metal isotope-tagged antibodies was used to characterize the hepatic immune compartment at days 1, 2, 3, and 7 after administration of MSCs or PBS. Results MSC treatment significantly alleviated CCl4-induced ALI and improved the survival rate. MSC treatment also modulated the hepatic immune system in terms of the distribution of immune-cell subsets and the phenotype of single cells. During the injured phase, MSCs inhibited a systemic response by reducing the numbers of Ly6ClowCD8+ TRM cells, conventional NK cells, and IgM+IgD+ B cells; suppressing the activation of Ly6ChiCD8+ TRM cells; downregulating MHC II and IgM expression in IgM+IgD+ B cells; and increasing the number of immunosuppressive monocyte-derived macrophages. During the recovery phase, MSCs promoted the retention of Ly6ClowCD8+ TRM cells and maintained the immunosuppressive activity of monocyte-derived macrophages. The response to MSC treatment differed between the injured and recovery phases, emphasizing the benefit of dynamic assessment of the immunomodulatory effects of MSCs. Conclusions We determined the immunomodulatory effects of MSC treatment on the subtype distribution and phenotypes of hepatic immune cells. Electronic supplementary material The online version of this article (10.1186/s13287-019-1379-6) contains supplementary material, which is available to authorized users.

Ferric modified chromium (III)-fibrous protein (Fe–CrFP) sorbent for phosphate and fluoride removal was prepared through crosslinking reaction. This adsorbent was characterized by elemental analysis, X-ray diffraction (XRD), Scanning electron microscope (SEM), Fourier Transform infrared spectroscopy (FTIR) and zeta potential. Results indicated that Fe–CrFP possessed good adsorption ability for both phosphate and fluoride due to its higher isoelectric point (pH = 9.2). Phosphate and fluoride had different pH dependence on solution pH: phosphate removal decreased rapidly beyond pH = 6.0, while a higher fluoride sorption amount was obtained in a pH range of 3.0–9.0. Adsorption isotherms for PO43− and F− were well described by the Langmuir equation. XRD analysis illustrated that Fe(III) on Fe–CrFP was amorphous, and hydrous ferric oxide formed on Fe–CrFP played an important role in adsorption. The main adsorption mechanisms of phosphate and fluoride were attributed to electrostatic attraction, additionally Fe–CrFP could also capture phosphate and fluoride through specific adsorption with formation of inner-sphere complex by surface hydroxyl groups (Fe–OH). Fluoride was easier to be influenced by coexisting anions in comparison to PO43−, and competitive sorption occurred in F− in presence of PO43−. Phosphate and fluoride adsorbed on Fe–CrFP could be totally desorbed by alkali solution, recycling experiment suggested that Fe–CrFP had a good utilization in treatment of phosphate and fluoride and provided a possibly valuable application for tanning leather waste.

Coronary artery bypass graft (CABG) has been confirmed to effectively improve the prognosis of coronary artery disease, which is a major public health concern worldwide. As the most frequently used conduits in CABG, saphenous vein grafts have the disadvantage of being susceptible to restenosis due to intimal hyperplasia. To meet the urgent clinical demand, adopting external stents (eStents) and illuminating the potential mechanisms underlying their function are important for preventing vein graft failure. Here, using 4-axis printing technology, we fabricated a novel biodegradable and flexible braided eStent, which exerts excellent inhibitory effect on intimal hyperplasia. The stented grafts downregulate Yes-associated protein (YAP), indicating that the eStent regulates vein graft remodeling via the Hippo-YAP signaling pathway. Further, as a drug-delivery vehicle, a rapamycin (RM)-coated eStent was designed to amplify the inhibitory effect of eStent on intimal hyperplasia through the synergistic effects of the Hippo and mammalian target of rapamycin (mTOR) signaling pathways. Overall, this study uncovers the underlying mechanisms of eStent function and identifies a new therapeutic target for the prevention of vein graft restenosis.

Rationale:Traumatic neuroma is a reparative proliferative response of the nerve after trauma or surgery, which rarely occurs in the breast. However, it must be distinguished from tumor recurrence.Patient concerns:A 78-year-old woman underwent left-sided modified radical mastectomy for invasi