Small bowel adenocarcinoma of the jejunum detected by double contrast enhanced ultrasound: a case report of a novel ultrasound modality.

Background: Small Bowel Adenocarcinoma (SBA) is rare, occult and life-threatening malignancy in digestive system. Given low incidence and nonspecific symptoms, SBA is frequently detected in later stages. Double contrast enhanced ultrasound (DCEUS) is an innovative imaging technique applied to visualize the gastrointestinal tract, merging intravenous contrast-enhanced ultrasound with oral contrast-enhanced ultrasound. In this case, DCEUS was utilized and successfully detected an SBA of the jejunum. Case presentation: A Chinese woman, aged 64, sought consultation in the gastroenterology department at our hospital, reporting symptoms of abdominal pain. Three months before entering the hospital, she underwent gastroscopy and colonoscopy which suggested chronic gastritis, and she was treated with oral drugs. However, her symptoms were not relieved, and even worsened. To further investigate, DCEUS was performed. The oral contrast agent dilated the luminal space of the upper gastrointestinal tract, resolving the hindrance caused by gas in the gastrointestinal tract and creating an acoustic window for scanning. Through this acoustic window, oral agent contrast-enhanced ultrasound (OA-CEUS) revealed a localized thickening of jejunal intestinal wall measuring 4x3 cm. Following intravenous injection of ultrasound contrast agent, the jejunal lesion exhibited faster enhancement and heterogeneous hyper-enhancement. Finally, the patient underwent jejunal tumor resection. Pathological examination revealed a jejunal adenocarcinoma. Conclusion: The timely diagnosis of SBA can be challenging. DCEUS may have the potential to contribute to diagnosis and detailed evaluation of SBA, particularly in cases involving jejunum. Further researches are needed to fully explore the benefits of DCEUS in the standard diagnostic approach for small bowel diseases.

Proteome-wide mendelian randomization investigates potential associations in heart failure and its etiology: emphasis on PCSK9.

BACKGROUND: Heart failure (HF) is a prevalent clinical syndrome with diverse etiologies. It is crucial to identify novel therapeutic targets based on underlying causes. Here, we aimed to use proteome-wide Mendelian randomization (MR) analyses to identify the associations between genetically predicted elevated levels of circulating proteins and distinct HF outcomes, along with specific HF etiologies. METHODS: Protein quantitative trait loci (pQTL) data for circulating proteins were sourced from the Atherosclerosis Risk in Communities (ARIC) study, encompassing 7,213 individuals and profiling 4,657 circulating proteins. Genetic associations for outcomes were obtained from the HERMES Consortium and the FinnGen Consortium. Colocalization analysis was employed to assess the impact of linkage disequilibrium on discovered relationships. For replication, two-sample MR was conducted utilizing independent pQTL data from the deCODE study. Multivariable MR (MVMR) and two-step MR were further conducted to investigate potential mediators. RESULTS: Two proteins (PCSK9 and AIDA) exhibited associations with HF in patients with coronary heart disease (CHD), and four proteins (PCSK9, SWAP70, NCF1, and RELT) were related with HF in patients receiving antihypertensive medication. Among these associations, strong evidence from subsequent analyses supported the positive relationship between genetically predicted PCSK9 levels and the risk of HF in the context of CHD. Notably, MVMR analysis revealed that CHD and LDL-C did not exert a complete mediating effect in this relationship. Moreover, two-step MR results yielded valuable insights into the potential mediating proportions of CHD or LDL-C in this relationship. CONCLUSIONS: Our findings provide robust evidence supporting the association between PCSK9 and concomitant HF and CHD. This association is partly elucidated by the influence of CHD or LDL-C, underscoring the imperative for additional validation of this connection and a thorough exploration of the mechanisms through which PCSK9 directly impacts ischemic HF.

Correlation between the prognostic nutritional index and outcomes in older patients aged ≥ 60 years with chronic heart failure.

BACKGROUND: Nutritional status is related to clinical outcomes in patients with chronic heart failure (CHF). The prognostic nutritional index (PNI) is a simple tool to assess nutrition. AIM: To evaluate the association between the PNI score and clinical outcomes in patients (60 years and older) hospitalized due to an acute exacerbation of CHF. METHOD: This was a retrospective observational study. Patients hospitalized for acute CHF exacerbation between July 2015 and May 2020 were analyzed. Patients were followed until January 31, 2021. The primary end point was cardiovascular-related readmissions and all-cause mortality after hospital discharge. Secondary outcomes were factors associated with all-cause mortality. Patients were divided into normal nutrition (PNI > 38), moderate malnutrition (PNI = 35-38), and severe malnutrition (PNI < 35) groups. RESULTS: The study included 355 patients (mean age 78 ± 9 years). The median follow-up was 769 days. Compared to survivors (n = 214), patients who expired (n = 133) were (1) older; (2) had lower PNI scores, lymphocyte counts, hemoglobin, albumin, total cholesterol, and serum sodium level; but (3) had higher serum creatinine levels, log(N-terminal-pro-B-type natriuretic peptide), and cardiac troponin I (P < 0.05). Multivariate analyses revealed that PNI was independently associated with all-cause mortality. The hazard ratio (HR) for moderate malnutrition versus normal nutrition was 1.624 (95% confidence interval [CI] 1.011-2.609, P = 0.045), while HR for severe malnutrition versus normal nutrition was 1.892 (95%CI 1.119-3.198, P = 0.017). Malnourished patients had significantly higher rates of cardiovascular readmissions and all-cause mortality. CONCLUSION: Lower PNI (malnutrition) was associated with worse clinical outcomes and was independently associated with all-cause mortality in patients with CHF.

Abnormal ECG detection based on an adversarial autoencoder.

Automatic detection and alarm of abnormal electrocardiogram (ECG) events play an important role in an ECG monitor system; however, popular classification models based on supervised learning fail to detect abnormal ECG effectively. Thus, we propose an ECG anomaly detection framework (ECG-AAE) based on an adversarial autoencoder and temporal convolutional network (TCN) which consists of three modules (autoencoder, discriminator, and outlier detector). The ECG-AAE framework is trained only with normal ECG data. Normal ECG signals could be mapped into latent feature space and then reconstructed as the original ECG signal back in our model, while abnormal ECG signals could not. Here, the TCN is employed to extract features of normal ECG data. Then, our model is evaluated on an MIT-BIH arrhythmia dataset and CMUH dataset, with an accuracy, precision, recall, F1-score, and AUC of 0.9673, 0.9854, 0.9486, 0.9666, and 0.9672 and of 0.9358, 0.9816, 0.8882, 0.9325, and 0.9358, respectively. The result indicates that the ECG-AAE can detect abnormal ECG efficiently, with its performance better than other popular outlier detection methods.

Mental Health of Chinese People During the COVID-19 Pandemic: Associations With Infection Severity of Region of Residence and Filial Piety.

This study aims to investigate mental health among Chinese people living in areas with differing levels of infection severity during the COVID-19 outbreak. It also assesses the association between reciprocal and authoritarian filial piety and mental health in times of crises. A sample of 1,201 Chinese participants was surveyed between April and June 2020. Wuhan city (where 23.4% of participants resided), Hubei province outside Wuhan (13.4% of participants), and elsewhere in China (63.1% of participants) were categorized into high, moderate, and low infection severity areas, respectively. The Depression, Anxiety, and Stress Scale's severity cut-points were used to categorize participants. In the overall sample, 20.9, 34.2, and 29.0% of the participants showed elevated (mild to extremely severe) levels of stress, anxiety, and depression. Those in the highest infection severity group were significantly more likely to be categorized as having elevated levels of stress, anxiety, and depression. General linear modeling was performed on a composite mental distress variable (taking into account stress, anxiety, and depression scores). This model indicated that, even after adjusting for group differences in age, gender, education, and filial piety, the high infection severity group displayed more mental distress than the low infection severity groups. The model also found reciprocal filial piety to have a negative association with mental distress. Conversely, authoritarian filial piety was found to be unrelated to mental distress when controlling for the other variables in the model. No evidence was found for an interaction between either authoritarian or reciprocal filial piety and infection severity, which suggests that the negative association observed between reciprocal filial piety and mental distress was relatively consistent across the three infection severity groups. The findings suggest that future public health programs may integrate the promotion of filial piety as a strategy to help Chinese people maintain good mental health in the face of pandemic crises.

Assembly Pathway Selection with DNA Reaction Circuits for Programming Multiple Cell-Cell Interactions.

The manipulation of cell-cell interactions promotes the study of multicellular behavior, but it remains a great challenge for programming multicellular assembly in complex reaction pathways with multiple cell types. Here we report a DNA reaction circuit-based approach to cell-surface engineering for the programmable regulation of multiple cell-cell interactions. The DNA circuits are designed on the basis of a stem-loop-integrated DNA hairpin motif, which has the capability of programming diverse molecular self-assembly and disassembly pathways by sequential allosteric activation. Modifying the cell surface with such DNA reaction circuits allows for performing programmable chemical functions on cell membranes and the control of multicellular self-assembly with selectivity. We demonstrate the selective control of targeting the capability of natural killer (NK) cells to two types of tumor cells, which show selectively enhanced cell-specific adaptive immunotherapy efficacy. We hope that our method provides new ideas for the programmable control of multiple cell-cell interactions in complex reaction pathways and potentially promotes the development of cell immunotherapy.

Co­expression of tissue kallikrein 1 and tissue inhibitor of matrix metalloproteinase 1 improves myocardial ischemia­reperfusion injury by promoting angiogenesis and inhibiting oxidative stress.

Myocardial ischemia/reperfusion (I/R) injury is a serious complication of reperfusion therapy for myocardial infarction. At present, there is not an effective treatment strategy available for myocardial I/R. The present study aimed to investigate the effects of human tissue kallikrein 1 (hTK1) and human tissue inhibitors of matrix metalloproteinase 1 (hTIMP1) gene co­expression on myocardial I/R injury. A rat model of myocardial I/R injury and a cell model with hypoxia/reoxygenation (H/R) treatment in cardiac microvascular endothelial cells (CMVECs) were established, and treated with adenovirus (Ad)­hTK1/hTIMP1. Following which, histological and triphenyl­tetrazolium­chloride staining assays were performed. Cardiac function was tested by echocardiographic measurement. The serum levels of oxidative stress biomarkers in rats and the intracellular reactive oxygen species (ROS) levels in CMVECs were measured. Additionally, experiments, including immunostaining, reverse transcription­quantitative PCR, western blotting, and MTT, wound healing, Transwell and tube formation assays were also performed. The results of the present study demonstrated that Ad­hTK1/hTIMP1 alleviated myocardial injury and improved cardiac function in myocardial I/R model rats. Ad­hTK1/hTIMP1 also significantly enhanced microvessel formation, decreased matrix metalloproteinase (MMP)2 and MMP9 expression, and reduced oxidative stress in myocardial I/R model rats. Furthermore, Ad­hTK1/hTIMP1 significantly enhanced proliferation, migration and tube formation in H/R­treated CMVECs. Additionally, Ad­hTK1/hTIMP1 significantly decreased intracellular ROS production and γ­H2A.X variant histone expression levels in H/R­treated CMVECs. In conclusion, the results of the present study demonstrated that co­expression of hTK1 and hTIMP1 genes displayed significant protective effects on myocardial I/R injury by promoting angiogenesis and suppressing oxidative stress; therefore, co­expression of hTK1 and hTIMP1 may serve as a potential therapeutic strategy for myocardial I/R injury.

Novelty Seeking and Mental Health in Chinese University Students Before, During, and After the COVID-19 Pandemic Lockdown: A Longitudinal Study.

COVID-19 has created significant concern surrounding the impact of pandemic lockdown on mental health. While the pandemic lockdown can be distressing, times of crisis can also provide people with the opportunity to think divergently and explore different activities. Novelty seeking, where individuals explore novel and unfamiliarly stimuli and environments, may enhance the creativity of individuals to solve problems in a way that allows them to adjust their emotional responses to stressful situations. This study employs a longitudinal design to investigate changes in novelty seeking and mental health outcomes (namely, stress, anxiety, and depression) before, during, and after COVID-19 pandemic lockdown, among a group of students (final N = 173; M age = 19.81; SD age = 0.98; 135 females and 38 males) from a university in southeast China. Participants were surveyed at three points: November, 2019 (prior to the COVID-19 pandemic); between February and March, 2020 (during the peak of the pandemic and intense lockdown in China); and between May and June, 2020 (after lockdown had been lifted in China). Cross-sectionally, correlation analysis indicated that greater novelty seeking was associated with lower levels of stress, anxiety, and depression at all three time points. Univariate latent curve modeling (LCM) indicated a growth trajectory in which novelty seeking increased over time and then remained high during the post-lockdown period. Stress, anxiety, and depression all showed V-shaped growth trajectories in which these variables decreased during lockdown, before increasing in the post-lockdown period. Multivariate LCM indicated the growth trajectory for novelty seeking was associated with the growth trajectories for stress, anxiety, and depression. This suggests that the observed decreases in stress, anxiety, and depression during the lockdown period may be attributable to the sample's observed increase in novelty seeking. These findings are valuable in that they challenge the notion that lockdown measures are inherently detrimental to mental health. The findings indicate the important role of novelty seeking in responding to crises. It may be possible for future public health measures to incorporate the promotion of novelty seeking to help individuals' respond to stressful situations and maintain good mental health in the face of crises.

Exploration of the effect of salvianolate on myocardial infarction in rats based on tandem mass tags.

Salvianolate is a compound from traditional Chinese medicine widely used in the treatment of various cardiovascular diseases. This study explored the effects of salvianolate on myocardial infarction and used tandem mass tags (TMT) to discover differentially expressed proteins. Male Sprague Dawley rats were randomly divided into the sham operation group, model group, and salvianolate group. The myocardial infarction model was established by ligating the left anterior descending coronary artery while the sham group had a sham operation. The rats were intraperitoneally injected with 2 ml of 5% glucose once a day, with 48.438 mg/kg/d salvianolate for the rats in the salvianolate group. After 4 weeks, the rats' hemodynamics were measured to evaluate cardiac function, and Masson staining assessed the area of myocardial infarction. TMT analysis was performed and validated by western blot. Salvianolate improved cardiac function after myocardial infarction, reduced the myocardial infarction area, and protected the myocardial tissue. 100 differentially expressed proteins were identified between the sham operation and model groups, salvianolate reversed the expression of 25 of those proteins, that were mainly involved in the metabolism of extracellular collagen matrix and the response to growth factor stimulation. Type I collagen, type V collagen, chymase, ß-myosin heavy chain, and A-Raf differential expression were consistent in western blotting. In conclusion, salvianolate had a protective effect on myocardial tissues of rats with myocardial infarction. Several proteins including type I collagen, type V collagen, chymase, ß-myosin, and A-Raf may be salvianolate targets for treatment of myocardial infarction.

[Corrigendum] Protective effect of sonic hedgehog against oxidized low­density lipoprotein-induced endothelial apoptosis: Involvement of NF-κB and Bcl-2 signaling.

Following the publication of this article, the authors have realized that the affiliation for the first author, Huashan Huang, was presented incorrectly as a multiple affiliation: Because the student was under the supervision of Professor Pengli Zhu, the only affiliation that should have been presented in this paper for this author was for the first affiliation, i.e., Shengli Clinical Medical college of Fujian Medical University. Therefore, the author affiliations for this paper should have appeared as follows: HUASHAN HUANG1, HUIZHEN YU1-3, LIANG LIN4, JUNMING cHEN1,2 and PENGLI ZHU1,2 1Shengli Clinical Medical College of Fujian Medical University; 2Key Laboratory of Geriatrics, Fujian Provincial Hospital, Fuzhou, Fujian 350001; Departments of 3Cardiology and 4Gynecology and Obstetrics, Fujian Provincial Hospital South Branch, Fuzhou, Fujian 350028, P.R. China. [the original article was published in International Journal of Molecular Medicine 45: 1864-1874, 2020; DOI: 10.3892/ijmm.2020.4542].

Comparison of predictive value of NT-proBNP, sST2 and MMPs in heart failure patients with different ejection fractions.

BACKGROUND: This study sought to compare the predictive value of NT-proBNP, sST2 and MMPs in HF with different ejection fractions from a population in southern China. METHODS: A cross-sectional study was conducted on 113 HF patients admitted to Fujian Provincial Hospital from December 2016 to March 2018.The patients were divided into three subgroups: 60 cases in HFpEF group (LVEF≥50%), 28 cases in HFmrEF group (41% ≤ LVEF≤49%) and 25 cases in HFrEF group (LVEF≤40%). ELISA method was applied to detect the concentrations of sST2, MMP-2 and MMP-9. Electrochemical luminescence immunoassay was applied to detect the concentration of plasma NT-proBNP. Univariate and multivariate Cox and logistic regression models were used to analyze the diagnostic significance of these plasma biomarkers in HF patients. Kaplan-Meier survival curves were used to assess the prognostic value of sST2 in the incidence of long-term adverse events during study. RESULTS: This study showed that plasma sST2 levels in HFrEF or HFmrEF patients were significantly higher than in HFpEF patients. Plasma levels of MMP-2 and MMP-9 in HFrEF patients were apparently higher than in HFpEF or HFmrEF patients. For the diagnosis of HFpEF, the AUC of NT-proBNP was higher than that of sST2, MMP-2 and MMP-9, which were 0.881, 0.717, 0.705 and 0.597, respectively. For the diagnosis of HFmrEF, the AUC of plasma sST2 was higher than that of MMP-2, MMP-9 and NT-proBNP, which were 0.799, 0.678, 0.676 and 0.793, respectively. For the diagnosis of HFrEF, the AUC of plasma NT-proBNP, sST2, MMP-2, and MMP-9 were 0.945, 0.820, 0.814, and 0.774 respectively. Spearman correlation analysis showed that plasma sST2 levels were significantly correlated with plasma MMP-2, MMP-9 and NT-proBNP levels. Further logistic regression analysis showed that except MMP-9, the biomarkers sST2 (OR = 1.960), MMP-2 (OR = 0.805) and NT-proBNP (OR = 0.002) were all independent risk factors for patients with heart failure. Survival analysis results suggested that for patients with HFmrEF, a higher level of plasma sST2 (≥ 0.332 ng/ml at admission) may predict a higher risk of endpoint events and a lower survival rate (P < 0.025). CONCLUSIONS: The circulating biomarkers sST2, MMP-2 and NT-proBNP were all independent risk factors for patients with heart failure. The sST2 can be a useful biomarker with both diagnostic and prognostic value in patients with HFmrEF. The higher sST2 level in patients with heart failure was related to a higher incidence of combined endpoint outcome.

Circular RNA circ-RELL1 regulates inflammatory response by miR-6873-3p/MyD88/NF-κB axis in endothelial cells.

Endothelial inflammation is an important contributor to the pathology of atherosclerotic cardiovascular disease (ASCVD). Circular RNAs (circRNAs) function and role in endothelium inflammation still unknown. In our present study, we firstly identified that circ-RELL1 plays a proinflammatory role in ox-LDL-induced HUVECs through high-throughput circRNA microarray assays. Knockdown circ-RELL1 can reduce the expression of ICAM1 and VCAM1 in ox-LDL induced endothelium inflammation. Mechanistically, circ-RELL1 directly bound to miR-6873-3p in cytoplasm. Subsequently miR-6873-3p reduced MyD88 (myeloid differentiation primary response 88) protein expression and alleviated MyD88 medicated NF-κB activation. Furthermore, circ-RELL1 can abolish the inhibition of inflammation response by miR-6873-3p. Our findings illustrate a novel regulatory pathway that circ-RELL1 modulate inflammatory response by miR-6873-3p/MyD88/NF-κB axis in ox-LDL induced endothelial cells, which provides a potential therapeutic candidate for endothelium inflammation in atherosclerotic cardiovascular disease.

Protective effect of sonic hedgehog against oxidized low­density lipoprotein­induced endothelial apoptosis: Involvement of NF­κB and Bcl­2 signaling.

Sonic hedgehog (Shh) is pivotally important in embryonic and adult blood vessel development and homeostasis. However, whether Shh is involved in atherosclerosis and plays a role in endothelial apoptosis induced by oxidized low­density lipoprotein (ox­LDL) has not been reported. The present study used recombinant Shh­N protein (rShh­N) and a plasmid encoding the human Shh gene (phShh) to investigate the role of Shh in ox­LDL­mediated human umbilical vein endothelial cell (HUVEC) apoptosis. The present study found that ox­LDL was able to induce apoptosis in HUVECs and that Shh protein expression was downregulated. Furthermore, pretreatment with rShh­N or transfection with phShh increased anti­apoptosis protein Bcl­2 expression and decreased cell apoptosis. These protective effects of rShh­N could be abolished by cyclopamine, which is a hedgehog signaling inhibitor. Furthermore, a co­immunoprecipitation assay was performed to demonstrate that Shh interacted with NF­κB p65 in HUVECs. Additionally, ox­LDL upregulated the phosphorylation of NF­κB p65 and inhibitor of NF­κB­α (IκBα), and these effects decreased notably following rShh­N and phShh treatment. Together, the present findings suggested that Shh serves an important protective role in alleviating ox­LDL­mediated endothelial apoptosis by inhibiting the NF­κB signaling pathway phosphorylation and Bcl­2 mediated mitochondrial signaling.

A Self-Calibrating Surface-Enhanced Raman Scattering-Active System for Bacterial Phenotype Detection.

Pathogen detection is of significant importance in human health and safety due to the high morbidity and mortality induced by bacterial infections. Therefore, the development of rapid, sensitive, and selective methods for the discrimination of pathogens is the key to improve the patient survival rates. In this work, we develop a new self-calibrating surface-enhanced Raman scattering (SERS)-based sensor that enables sensitive and reproducible pathogen detection in practical samples. The assay makes use of gold nanoflowers (AuNFs) consisting of three components: a solid Au core of ∼15 nm, a hollow gap of ∼1 nm, and a flower-like Au shell. We have demonstrated that the sensitive and quantitative analysis of biomolecules can be achieved by the target-dependent, sequence-specific DNA hybridization assembly between AuNFs with a built-in internal standard. We further demonstrate that this kind of reliable SERS sensor is able to distinguish different bacteria with sensitivity down to single bacterium. We expect that the established quantitative SERS technique could provide a promising tool for widespread applications in biomedical research and clinical diagnostics.

Screening Analysis of Sirtuins Family Expression on Anti-Inflammation of Resveratrol in Endothelial Cells.

BACKGROUND Resveratrol has been shown to possess beneficial activities including antioxidant, anti-inflammatory, and cardioprotective effects through activating a nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase family member sirtuin-1 (SIRT1) protein. The current study was undertaken to investigate the role of sirtuin family members (SIRT1-SIRT7) on the anti-inflammation activities of resveratrol in endothelial cells. MATERIAL AND METHODS Primary human umbilical vein endothelial cells (HUVECs) were pretreated with resveratrol before tumor necrosis factor (TNF)-alpha (10-20 µg/L) stimulation. Cell viability was measured using the Cell Counting Kit-8 method. Total RNA was extracted after different treatments and the NimbleGen Human 12×135K Gene Expression Array was applied to screen and analyze SIRTs expression. Quantitative real-time polymerase chain reaction and western blot were applied to verify the results of the gene expression microarrays. Reactive oxygen species (ROS) production was examined using flow cytometry analysis. RESULTS Microarray analysis showed that the expressions of SIRT1, SIRT2, SIRT3, SIRT5, SIRT6, and SIRT7 showed the tendency to increase while SIRT4 showed the tendency to decrease. SIRT1, SIRT2, SIRT5, and SIRT7 gene expression could be upregulated by pretreatment with resveratrol compared with TNF-alpha alone while there were no obvious differences of SIRT3, SIRT4, and SIRT6 expressions observed in TNF-alpha alone treated cells and resveratrol-TNF-alpha co-treated cells. Interestingly, SIRT1, SIRT2, SIRT3, SIRT4, and SIRT5 siRNA could reverse the effect of resveratrol on ROS production; SIRT1 and SIRT5 siRNA could significantly increase CD40 expression inhibited by resveratrol in TNF-a treated cells. CONCLUSIONS Our results suggest that resveratrol inhibiting oxidative stress production is associated with SIRT1, SIRT2, SIRT3, SIRT4, and SIRT5 pathways; attenuating CD40 expression was only associated with SIRT1 and SIRT5 pathways in TNF-alpha-induced endothelial cells injury.

Self-Assembly of Metallo-Nucleoside Hydrogels for Injectable Materials That Promote Wound Closure.

Injectable hydrogels are increasingly being used as scaffolds for in situ tissue engineering and wound healing. Most of these injectable hydrogels are made from polymers, and there are fewer examples of such soft materials made via self-assembly of low-molecular weight gelators. We report the room-temperature synthesis of a functional hydrogel formed by mixing cytidine (C) with 0.5 equiv each of B(OH)3 and AgNO3. The structural basis for this supramolecular hydrogel (C-B-C·Ag+) involves orthogonal formation of cytidine borate diesters (C-B-C) and Ag+-stabilized C-C base pairs, namely, the C·Ag+·C dimer. The C-B-C·Ag+ hydrogels, which can have high water content (at least 99.6%), are stable (no degradation after 1 year in the light), stimuli-responsive, and self-supporting, with elastic moduli of up to 104 Pa. Incorporation of Ag+ ions into the gel matrix endows the C-B-C·Ag+ hydrogel with significant antibacterial capability. Importantly, the rapid switching between the sol and gel states for this supramolecular hydrogel, as a response to shear stress, enables 3D printing of a flexible medical patch made from the C-B-C·Ag+ hydrogel. The C-B-C·Ag+ hydrogel was used to promote the closure of burn wounds in a mouse model.

Peptide self-assembly assisted signal labeling for an electrochemical assay of protease activity.

Peptide self-assembly holds tremendous promise for a range of applications in chemistry and biology. In the work reported here, we explored the potential functions of peptide self-assembly in electrochemical bioanalysis by developing a peptide self-assembly assisted signal labeling strategy for assaying protease activity. The fundamental principle of this assay is that target-protease-catalyzed specific proteolytic cleavage blocks self-assembly between the probe peptide and signal peptide, thus preventing the signal labeling of electroactive silver nanoparticles on the electrode surface, which in turn causes the electrochemical signal to decrease. Using trypsin as an example protease target, the linear range of this assay was found to be 1 ng mL-1 to 100 mg mL-1, and its detection limit was 0.032 ng mL-1, which are better than the corresponding parameters for previously reported assays. Further experiments also highlighted the good selectivity of the assay method and demonstrated its usability when applied to serum samples. Therefore, this report not only introduces a valuable tool for assaying protease activity, but it also promotes the utilization of peptide self-assembly in electrochemical bioanalysis, as this approach has great potential for practical use in the future.

Triblock copolymers encapsulated poly (aryl benzyl ether) dendrimer zinc(II) phthalocyanine nanoparticles for enhancement in vitro photodynamic efficacy.

A novel series of nanoparticles formed via an electrostatic interaction between the periphery of negatively charged 1-2 generation aryl benzyl ether dendrimer zinc (II) phthalocyanines and positively charged poly(L-lysin) segment of triblock copolymer, poly(L-lysin)-block-poly(ethylene glycol)-block-poly(L-lysin), was developed for the use as an effective photosensitizers in photodynamic therapy. The dynamic light scattering, atomic force microscopy showed that two nanoparticles has a relevant size of 80-150nm. The photophysical properties and singlet oxygen quantum yields of free dendrimer phthalocyanines and nanoparticles exhibited generation dependence. The intracellular uptake of dendrimer phthalocyanines in Hela cells was significantly elevated as they were incorporated into the micelles, but was inversely correlated with the generation of dendrimer phthalocyanines. The photocytotoxicity of dendrimer phthalocyanines incorporated into polymeric micelles was also increased. The presence of nanoparticles induced efficient cell death. Using a mitochondrial-sepcific dye rhodamine 123 (Rh123), our fluorescence microscopic result indicated that nanoparticles localized to the mitochondria.