Distributed continuous-time accelerated neurodynamic approaches for sparse recovery via smooth approximation to L1-minimization.

This paper develops two continuous-time distributed accelerated neurodynamic approaches for solving sparse recovery via smooth approximation to L1-norm minimization problem. First, the L1-norm minimization problem is converted into a distributed smooth optimization problem by utilizing multiagent consensus theory and smooth approximation. Then, a distributed primal-dual accelerated neurodynamic approach is designed by using Karush-Kuhn-Tucker (KKT) condition and Nesterov's accelerated method. Furthermore, in order to reduce the structure complexity of the presented neurodynamic approach, based on the projection matrix, we eliminate a dual variable in the KKT condition and propose a distributed accelerated neurodynamic approach with a simpler structure. It is proved that the two proposed distributed neurodynamic approaches both achieve O(1t2) convergence rate. Finally, the simulation results of sparse recovery are given to demonstrate the effectiveness of the proposed approaches.

AKAP1 in Renal Patients with AHF to Reduce Ferroptosis of Cardiomyocyte.

BACKGROUND: This study mainly investigated the mechanism and effects of AKAP1 in renal patients with acute heart failure (AHF). METHODS: Patients with renal patients with AHF and normal volunteers were collected. The left anterior descending arteries (LAD) of mice were ligated to induce myocardial infarction. RESULTS: AKAP1 messenger RNA (mRNA) expression was found to be down-regulated in renal patients with AHF. The serum levels of AKAP1 mRNA expression were negatively correlated with collagen I/III in patients. AKAP1 mRNA and protein expression in the heart tissue of mice with AHF were also found to be down-regulated in a time-dependent manner. Short hairpin (Sh)-AKAP1 promotes AHF in a mouse model. AKAP1 up-regulation reduces reactive oxygen species (ROS)-induced oxidative stress in an In Vitro model. AKAP1 up-regulation also reduces ROS-induced lipid peroxidation ferroptosis in an In Vitro model. AKAP1 induces NDUFS1 expression to increase GPX4 activity levels. AKAP1 protein interlinked with the NDUFS1 protein. Up-regulation of the AKAP1 gene reduced NDUFS1 ubiquitination, while down-regulation of the AKAP1 gene increased NDUFS1 ubiquitination in a model. In vivo imaging showed that the sh-AKAP1 virus reduced NDUFS1 expression in the heart of a mouse model. CONCLUSIONS: AKAP1 reduced ROS-induced lipid peroxidation ferroptosis through the inhibition of ubiquitination of NDUFS by mitochondrial damage in model of renal patients with AHF, suggest a novel target for AHF treatment.

PAllidal versus SubThalamic deep brain Stimulation for Cervical Dystonia (PASTS-CD): study protocol for a multicentre randomised controlled trial.

INTRODUCTION: Deep brain stimulation (DBS) has been validated as a safe and effective treatment for refractory cervical dystonia (CD). Globus pallidus internus (GPi) and subthalamic nucleus (STN) are the two main stimulating targets. However, there has been no prospective study to clarify which target is the better DBS candidate for CD. The objective of this trial is to compare directly the efficacy and safety of GPi-DBS and STN-DBS, thereby instructing the selection of DBS target in clinical practice. METHODS AND ANALYSIS: This multicentre, prospective, randomised, controlled study plans to enrol 98 refractory CD patients. Eligible CD patients will be randomly allocated to GPi-DBS group or STN-DBS group, with the DBS electrodes implanted into the posteroventral portion of GPi or the dorsolateral portion of STN, respectively. The primary outcome will be the improvement of symptomatic severity, measured by the changes in the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) severity subscale and the Tsui scale at 3 months, 6 months and 12 months after surgery. The secondary outcomes include the improvement of the TWSTRS-disability subscale, TWSTRS-pain subscale, quality of life, mental and cognitive condition, as well as the differences in stimulation parameters and adverse effects. In addition, this study intends to identify certain predictors of DBS efficacy for CD. ETHICS AND DISSEMINATION: The trial has been approved by the Medical Ethics Committee of Chinese PLA General Hospital (S2022-613-01). The results of this study will be published in international peer-reviewed journals and shared in professional medical conferences. TRIAL REGISTRATION NUMBER: NCT05715138.

[Panax notoginseng saponins improve monocrotaline-induced pulmonary arterial hypertension in rats by inhibiting ADAM10/Notch3 signaling pathway].

In this study, we investigated the effects of Panax notoginseng saponins (PNS) on pulmonary vascular remodeling and ADAM10/Notch3 pathway in pulmonary arterial hypertension (PAH). PAH rat model was established, and male Sprague Dawley (SD) rats were randomly divided into control group, monocrotaline (MCT) group and MCT+PNS group, with 10 rats in each group. Rats in the control group were intraperitoneally injected with equal volume of normal saline. Rats in the MCT group was injected intraperitoneally with 60 mg/kg MCT on the first day, and then with the same volume of normal saline every day. Rats in the MCT+PNS group was injected intraperitoneally with 60 mg/kg MCT on the first day, and then with 50 mg/kg PNS every day. The modeling time of each group lasted for 21 days. After the model was established, the mean pulmonary artery pressure (mPAP) was measured by right heart catheterization technique, the right ventricular hypertrophy index (RVHI) was calculated, the microscopic morphology and changes of pulmonary vascular wall were observed by HE and Masson staining, and the expressions of ADAM10, Notch3, Hes-1, P27, PCNA, Caspase-3 proteins and mRNA in pulmonary vascular tissue of rats were detected by Western blot and qPCR. The expression and localization of Notch3 and α-SMA were detected by immunofluorescence staining. The protein expression of ADAM10 was detected by immunohistochemical staining. The results showed that compared with the control group, mPAP, RVHI, pulmonary vessels and collagen fibers in the MCT group were significantly increased, the expressions of ADAM10, Notch3, Hes-1, and PCNA protein and mRNA were significantly increased, while the expressions of P27 and Caspase-3 protein and mRNA were decreased significantly. Compared with the MCT group, mPAP and RVHI were significantly decreased, pulmonary vessels were significantly improved and collagen fibers were significantly reduced, the expressions of protein and mRNA of ADAM10, Notch3, Hes-1, and PCNA were decreased in MCT+PNS group, but the expressions of protein and mRNA of P27 and Caspase-3 were increased slightly. The results of immunofluorescence showed that Notch3 and α-SMA staining could overlap, which proved that Notch3 was expressed in smooth muscle cells. The expression of Notch3 in the MCT group was increased significantly compared with that in the control group, while PNS intervention decreased the expression of Notch3. Immunohistochemical staining showed that compared with the control group, the amount of ADAM10 in the MCT group was increased significantly, and the expression of ADAM10 in the MCT+PNS group was decreased compared with the MCT group. These results indicate that PNS can improve the PAH induced by MCT in rats by inhibiting ADAM10/Notch3 signaling pathway.

Ischemia/reperfusion-activated ferroptosis in the early stage triggers excessive inflammation to aggregate lung injury in rats.

Objective: Lung ischemia/reperfusion injury (LIRI) is a clinical syndrome of acute lung injury that occurs after lung transplantation or remote organ ischemia. Ferroptosis and inflammation are involved in the pathogenesis of LIRI according to the results of several studies on animal models. However, the interactive mechanisms between ferroptosis and inflammation contributing to LIRI remain unclear. Methods: HE staining and indicators of oxidative stress were used to evaluated the lung injury. The reactive oxygen species (ROS) level was examined by DHE staining. The quantitative Real-time PCR (qRT-PCR) and western blot analysis were employed to detect the level of inflammation and ferroptosis, and deferoxamine (DFO) was used to assess the importance of ferroptosis in LIRI and its effect on inflammation. Results: In the present study, the link of ferroptosis with inflammation was evaluated at reperfusion 30-, 60- and 180-minute time points, respectively. As the results at reperfusion 30-minute point shown, the pro-ferroptotic indicators, especially cyclooxygenase (COX)-2 and acyl-CoA synthetase long-chain family member 4 (ACSL4), were upregulated while the anti-ferroptotic factors glutathione peroxidase 4 (GPX4), cystine-glumate antiporter (XCT) and ferritin heavy chain (FTH1) were downregulated. Meanwhile, the increased level of interleukin (IL)-6, tumor necrosis factor alpha (TNF-α) and IL-1ß were observed beginning at reperfusion 60-minute point but mostly activated at reperfusion 180-minute point. Furthermore, deferoxamine (DFO) was employed to block ferroptosis, which can alleviate lung injury. Expectedly, the survival rate of rats was increased and the lung injury was mitigated containing the improvement of type II alveolar cells ultrastructure and ROS production. In addition, at the reperfusion 180-minute point, the inflammation was observed to be dramatically inhibited after DFO administration as verified by IL-6, TNF-α and IL-1ß detection. Conclusion: These findings suggest that ischemia/reperfusion-activated ferroptosis plays an important role as the trigger for inflammation to further deteriorate lung damages. Inhibiting ferroptosis may have therapeutic potential for LIRI in clinical practice.

Enabling programmable dynamic DNA chemistry using small-molecule DNA binders.

The binding of small molecules to the double helical structure of DNA, through either intercalation or minor groove binding, may significantly alter the stability and functionality of DNA, which is a fundamental basis for many therapeutic and sensing applications. Here, we report that small-molecule DNA binders can also be used to program reaction pathways of a dynamic DNA reaction, where DNA strand displacement can be tuned quantitatively according to the affinity, charge, and concentrations of a given DNA binder. The binder-induced nucleic acid strand displacement (BIND) thus enables innovative technologies to accelerate the discovery and characterization of bioactive small molecules. Specifically, we demonstrate the comprehensive characterization of existing and newly discovered DNA binders, where critical parameters for binding affinity and sequence selectivity can be obtained in a single, unbiased molecular platform without the need for any specialized equipment. We also engineer a tandem BIND system as a high-throughput screening assay for discovering DNA binders, through which 8 DNA binders were successfully discovered from a library of 700 compounds.

Self-healing hydrogel as an injectable implant: translation in brain diseases.

Tissue engineering biomaterials are aimed to mimic natural tissue and promote new tissue formation for the treatment of impaired or diseased tissues. Highly porous biomaterial scaffolds are often used to carry cells or drugs to regenerate tissue-like structures. Meanwhile, self-healing hydrogel as a category of smart soft hydrogel with the ability to automatically repair its own structure after damage has been developed for various applications through designs of dynamic crosslinking networks. Due to flexibility, biocompatibility, and ease of functionalization, self-healing hydrogel has great potential in regenerative medicine, especially in restoring the structure and function of impaired neural tissue. Recent researchers have developed self-healing hydrogel as drug/cell carriers or tissue support matrices for targeted injection via minimally invasive surgery, which has become a promising strategy in treating brain diseases. In this review, the development history of self-healing hydrogel for biomedical applications and the design strategies according to different crosslinking (gel formation) mechanisms are summarized. The current therapeutic progress of self-healing hydrogels for brain diseases is described as well, with an emphasis on the potential therapeutic applications validated by in vivo experiments. The most recent aspect as well as the design rationale of self-healing hydrogel for different brain diseases is also addressed.

Relationship of Glycated Hemoglobin A1c with All-Cause and Cardiovascular Mortality among Patients with Hypertension.

Both low and high glycated hemoglobin A1c (HbA1c) levels are well-established causal risk factors for all-cause and cardiovascular mortality in the general population and diabetic patients. However, the relationship between HbA1c with all-cause and cardiovascular mortality among patients with hypertension is unclear. We used NHANES data from 1999 to 2014 as the basis for this population-based cohort study. Based on HbA1c levels (HbA1c > 5, HbA1c > 5.5, HbA1c > 6, HbA1c > 6.5, HbA1c > 7%), hypertensive patients were divided into five groups. An analysis of multivariable Cox proportional hazards was conducted based on hazard ratios (HRs) and respective 95% confidence intervals (CIs). The relationship between HbA1c and mortality was further explored using Kaplan-Meier survival curves, restricted cubic spline curves, and subgroup analyses. In addition, 13,508 patients with hypertension (average age 58.55 ± 15.56 years) were included in the present analysis, with 3760 (27.84%) all-cause deaths during a follow-up of 127.69 ± 57.9 months. A U-shaped relationship was found between HbA1c and all-cause and cardiovascular mortality (all p for likelihood ratio tests were 0.0001). The threshold value of HbA1c related to the lowest risk for all-cause and cardiovascular mortality was 5.3% and 5.7%, respectively. Below the threshold value, increased HbA1c levels reduced the risk of all-cause mortality (HR 0.68, 95% CI 0.51-0.90, p = 0.0078) and cardiovascular mortality (HR 0.77, 95% CI 0.57-1.05, p = 0.0969). Inversely, above the threshold value, increased HbA1c levels accelerated the risk of all-cause mortality (HR 1.14, 95% CI 1.11-1.18, p < 0.0001) and cardiovascular mortality (HR 1.22, 95% CI 1.16-1.29, p < 0.0001). In conclusion, A U-shape relationship was observed between HbA1c and all-cause and cardiovascular mortality among hypertensive patients.

How does HbA1c predict mortality and readmission in patients with heart failure? A protocol for systematic review and meta-analysis.

BACKGROUND: Accumulating evidence suggests that HbA1c levels, a common clinical indicator of chronic glucose metabolism over the preceding 2-3 months, are independent risk factors for cardiovascular disease, including heart failure. However, conflicting evidence obscures clear cutoffs of HbA1c levels in various heart failure populations. The aim of this review is to assess the possible predictive value and optimal range of HbA1c on mortality and readmission in patients with heart failure. METHODS: A systematic and comprehensive search will be performed using PubMed, Embase, CINAHL, Scopus, and the Cochrane Library databases before December 2022 to identify relevant studies. All-cause mortality is the prespecified primary endpoint. Cardiovascular death and heart failure readmission are secondary endpoints of interest. We will only include prospective and retrospective cohort studies and place no restrictions on the language, race, region, or publication period. The ROBINS-I tool will be used to assess the quality of each included research. If there were sufficient studies, we will conduct a meta-analysis with pooled relative risks and corresponding 95% confidence intervals to evaluate the possible predictive value of HbA1c for mortality and readmission. Otherwise, we will undertake a narrative synthesis. Heterogeneity and publication bias will be assessed. If heterogeneity was significant among included studies, a sensitivity analysis or subgroup analysis will be used to explore the source of heterogeneity, such as diverse types of heart failure or patients with diabetes and non-diabetes. Additionally, we will conduct meta-regression to examine the time-effect and treatment-effect modifiers on all-cause mortality compared between different quantile of HbA1c levels. Finally, a restricted cubic spline model may be used to explore the dose-response relationship between HbA1c and adverse outcomes. DISCUSSION: This planned analysis is anticipated to identify the predictive value of HbA1c for mortality and readmission in patients with heart failure. Improved understanding of different HbA1c levels and their specific effect on diverse types of heart failure or patients with diabetes and non-diabetes is expected to be figured out. Importantly, a dose-response relationship or optimal range of HbA1c will be determined to instruct clinicians and patients. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration details: CRD42021276067.

Antiviral and Antibacterial Sulfated Polysaccharide-Chitosan Nanocomposite Particles as a Drug Carrier.

Drug delivery system (DDS) refers to the method of delivering drugs to the targeted sites with minimal risk. One popular strategy of DDS is using nanoparticles as a drug carrier, which are made from biocompatible and degradable polymers. Here, nanoparticles composed of Arthrospira-derived sulfated polysaccharide (AP) and chitosan were developed and expected to possess the capabilities of antiviral, antibacterial, and pH-sensitive properties. The composite nanoparticles, abbreviated as APC, were optimized for stability of morphology and size (~160 nm) in the physiological environment (pH = 7.4). Potent antibacterial (over 2 µg/mL) and antiviral (over 6.596 µg/mL) properties were verified in vitro. The pH-sensitive release behavior and release kinetics of drug-loaded APC nanoparticles were examined for various categories of drugs, including hydrophilic, hydrophobic, and protein drugs, under different pH values of the surroundings. Effects of APC nanoparticles were also evaluated in lung cancer cells and neural stem cells. The use of APC nanoparticles as a drug delivery system maintained the bioactivity of the drug to inhibit the proliferation of lung cancer cells (with ~40% reduction) and to relieve the growth inhibitory effect on neural stem cells. These findings indicate that the pH-sensitive and biocompatible composite nanoparticles of sulfated polysaccharide and chitosan well keep the antiviral and antibacterial properties and may serve as a promising multifunctional drug carrier for further biomedical applications.

Bioactive self-healing hydrogel based on tannic acid modified gold nano-crosslinker as an injectable brain implant for treating Parkinson's disease.

BACKGROUND: Parkinson's disease (PD) is one of the most common long-term neurodegenerative diseases. Current treatments for PD are mostly based on surgery and medication because of the limitation and challenges in selecting proper biomaterials. In this study, an injectable bioactive hydrogel based on novel tannic acid crosslinker was developed to treat PD. METHODS: The oxidized tannic acid modified gold nano-crosslinker was synthesized and used to effectively crosslink chitosan for preparation of the bioactive self-healing hydrogel. The crosslinking density, conductivity, self-healing ability, and injectability of the hydrogel were characterized. Abilities of the hydrogel to promote the proliferation and differentiation of neural stem cells (NSCs) were assessed in vitro. Anti-inflammatory property was analyzed on J774A.1 macrophages. The hydrogel was injected in the PD rat model for evaluation of the motor function recovery, electrophysiological performance improvement, and histological repair. RESULTS: The hydrogel exhibited self-healing property and 34G (~ 80 µm) needle injectability. NSCs grown in the hydrogel displayed long-term proliferation and differentiation toward neurons in vitro. Besides, the hydrogel owned strong anti-inflammatory and antioxidative capabilities to rescue inflamed NSCs (~ 90%). Brain injection of the bioactive hydrogel recovered the motor function of PD rats. Electrophysiological measurements showed evident alleviation of irregular discharge of nerve cells in the subthalamic nucleus of PD rats administered with the hydrogel. Histological examination confirmed that the hydrogel alone significantly increased the density of tyrosine hydroxylase positive neurons and fibers as well as reduced inflammation, with a high efficacy similar to drug-loaded hydrogel. CONCLUSION: The new bioactive hydrogel serves as an effective brain injectable implant to treat PD and a promising biomaterial for developing novel strategies to treat brain diseases.

Enhancement of Cell Behavior by the Polysaccharide Extract of Arthrospira and Potential Biomedical Applications.

Arthrospira is one of the most studied cyanobacteria and has been reported with practical applications. Among the substances derived from Arthrospira, polysaccharides have received relatively less attention than phycocyanins, though they have more abundant structural variations and specific properties. Herein, a new Arthrospira-derived sulfated polysaccharide was explored for its potential bioactive functions. The ability of this sulfated polysaccharide to promote the behavior of neural stem cells (NSCs) in three-dimensional hydrogel was examined for the first time. NSCs encapsulated in the sulfated polysaccharide-containing hydrogel showed better proliferation than the control hydrogel as well as a unique cell clustering behavior, i.e., formation of multicellular spherical clusters (40-60 µm). The sulfated polysaccharide, in an appropriate range of concentration (5 mg/mL), also maintained the stemness of NSCs in hydrogel and facilitated their differentiation. In addition, the potentials of the new sulfated polysaccharide as a coating material and as a component for drug carrier were verified. The sulfated polysaccharide-modified substrate exhibited superhydrophilicity (contact angle ~9°) and promoted cell adhesion to the substrate. Composite nanoparticles composed of the sulfated polysaccharide and other differently charged polysaccharides were produced with an average diameter of ~240 nm and estimated drug loading of ~18%. The new Arthrospira-derived sulfated polysaccharide is a promising candidate for cell culture, surface-modification, and drug-delivery applications in the biomedical field.

Stretchable and biodegradable chitosan-polyurethane-cellulose nanofiber composites as anisotropic materials.

Chitosan is a naturally derived biodegradable polymer with abundancy, sustainability, and ease of chemical modification. Polyurethanes are a family of elastic biocompatible polymers, and composites of polyurethanes have versatile properties and applications. Chitosan-polyurethane composites were recently developed but had insufficient strength and limited stretchability. In the current study, cellulose nanofibers (CNFs) were integrated in chitosan-polyurethane composites to prepare stretchable and anisotropic materials. A biodegradable polyurethane was first synthesized, end-capped with aldehyde to become dialdehyde polyurethane (DP) nanoparticles, and added with CNFs to prepare the DP-CNF composite crosslinker (DPF). The waterborne DPF crosslinker was then blended with chitosan solution to make polyurethane-CNF-chitosan (DPFC) composites. After blending, DPFC may form hydrogel in ~33 min at room temperature, which confirmed crosslinking. Composite films cast and dried from the blends showed good elongation (~420.2 %) at 60 °C. Anisotropic films were then generated by tension annealing with pre-strain. The annealed films with 200 % pre-strain exhibited large elastic anisotropy with ~4.9 anisotropic ratio. In situ SAXS/WAXS analyses unveiled that rearrangement and alignment of the microstructure during tension annealing accounted for the anisotropy. The anisotropic composite films had the ability to orient the growth of neural stem cells and showed the potential for biomimetic and tissue engineering applications.

Systemic inflammation markers and the prevalence of hypertension: A NHANES cross-sectional study.

Systemic inflammation markers have been highlighted recently as related to cardiac and non-cardiac disorders. However, few studies have estimated pre-diagnostic associations between these markers and hypertension. In the National Health and Nutritional Examination Survey from 1999 to 2010, 22,290 adult participants were included for analysis. We assessed associations between four systemic inflammation markers based on blood cell counts: systemic immune-inflammation index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), and hypertension prevalence in multivariate logistic regression analysis with odds ratio (OR) and 95% confidence interval (CI). To further explore their associations, subgroup and sensitivity analyses were performed. In continuous analyses, the ORs for hypertension prevalence per ln-transformed increment in SII and NLR were estimated at 1.115 and 1.087 (95% CI: 1.045-1.188; 1.008-1.173; respectively). Compared to those in the lowest tertiles, the hypertension risks for subjects in the highest SII and NLR tertiles were 1.20 and 1.11 times, respectively. Conversely, we found that PLR and LMR were negatively associated with hypertension prevalence in continuous analyses (1.060, 0.972-1.157; 0.926, 0.845-1.014; respectively), and the highest PLR and LMR tertiles (1.041, 0.959-1.129; 0.943, 0.866-1.028; respectively). Also, subgroup and sensitivity analyses indicated that SII had a greater correlation to hypertension. In conclusion, we find positive associations between SII and NLR and the prevalence of hypertension in this cross-sectional study. Our findings highlight that SII may be a superior systemic inflammation warning marker for hypertension.

One-pass deep brain stimulation of subthalamic nucleus and ventral intermediate nucleus for levodopa-resistant tremor-dominant Parkinson's disease.

Objective: Tremor-dominant Parkinson's disease (TD-PD) can be further separated into levodopa-responsive and levodopa-resistant types, the latter being considered to have a different pathogenesis. Previous studies indicated that deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the globus pallidus internus (GPi) individually was not sufficient for tremor control, especially for the levodopa-resistant TD-PD (LRTD-PD). The thalamic ventral intermediate nucleus (VIM) has been regarded as a potent DBS target for different kinds of tremors. Therefore, we focused on the LRTD-PD subgroup and performed one-pass combined DBSs of STN and VIM to treat refractory tremors, aiming to investigate the safety and effectiveness of this one-trajectory dual-target DBS scheme. Methods: We retrospectively collected five LRTD-PD patients who underwent a one-pass combined DBS of STN and VIM via a trans-frontal approach. The targeting of VIM was achieved by probabilistic tractography. Changes in severity of symptoms (measured by the Unified Parkinson Disease Rating Scale part III, UPDRS-III), levodopa equivalent daily doses (LEDD), and disease-specific quality of life (measured by the 39-item Parkinson's Disease Questionnaire, PDQ-39) were evaluated. Results: Three-dimensional reconstruction of electrodes illustrated that all leads were successfully implanted into predefined positions. The mean improvement rates (%) were 53 ± 6.2 (UPDRS-III), 82.6 ± 11.4 (tremor-related items of UPDRS), and 52.1 ± 11.4 (PDQ-39), respectively, with a mean follow-up of 11.4 months. Conclusion: One-pass combined DBS of STN and VIM via the trans-frontal approach is an effective and safe strategy to alleviate symptoms for LRTD-PD patients.

Porous Structure of ß-Cyclodextrin for CO2 Capture: Structural Remodeling by Thermal Activation.

With a purpose of extending the application of ß-cyclodextrin (ß-CD) for gas adsorption, this paper aims to reveal the pore formation mechanism of a promising adsorbent for CO2 capture which was derived from the structural remodeling of ß-CD by thermal activation. The pore structure and performance of the adsorbent were characterized by means of SEM, BET and CO2 adsorption. Then, the thermochemical characteristics during pore formation were systematically investigated by means of TG-DSC, in situ TG-FTIR/FTIR, in situ TG-MS/MS, EDS, XPS and DFT. The results show that the derived adsorbent exhibits an excellent porous structure for CO2 capture accompanied by an adsorption capacity of 4.2 mmol/g at 0 °C and 100 kPa. The porous structure is obtained by the structural remodeling such as dehydration polymerization with the prior locations such as hydroxyl bonded to C6 and ring-opening polymerization with the main locations (C4, C1, C5), accompanied by the release of those small molecules such as H2O, CO2 and C3H4. A large amount of new fine pores is formed at the third and fourth stage of the four-stage activation process. Particularly, more micropores are created at the fourth stage. This revealed that pore formation mechanism is beneficial to structural design of further thermal-treated graft/functionalization polymer derived from ß-CD, potentially applicable for gas adsorption such as CO2 capture.

Gelation and the Self-Healing Behavior of the Chitosan-Catechol Hydrogel.

Mussel-inspired adhesive hydrogels have been developed in biomedical fields due to their strong adhesive property, cohesive capability, biocompatibility, and hemostatic ability. Catechol-functionalized chitosan is a potential polymer used to prepare adhesive hydrogels. However, the unique gelation mechanism and self-healing properties of catechol-grafted chitosan alone have not yet been explored. Herein, catechol-grafted chitosan (CC) was synthesized and further concentrated to obtain the self-healing CC hydrogels. The gelation mechanism of CC hydrogels may be attributed to the formation of hydrogen bonding, cation-π interactions, Michael addition, or Schiff base reactions during concentration phases. Rheological studies showed that the CC hydrogel owned self-healing properties in repeated damage-healing cycles. Coherent small-angle X-ray scattering (SAXS) analyses revealed the formation of a mesoscale structure (~9 nm) as the solid content of the hydrogel increased. In situ SAXS combined with rheometry verified the strain-dependent behavior of the CC hydrogel. The CC hydrogel displayed the osmotic-responsive behavior and enhanced adhesive strength (0.38 N/cm2) after immersion in the physiological saline. The CC scaffold prepared by lyophilizing the CC hydrogel revealed a macroporous structure (~200 µm), a high swelling ratio (9656%), good compressibility, and durability. This work provides an insight into the design of using chitosan-catechol alone to produce hydrogels or scaffolds with tunable mechanical properties for further applications in biomedical fields.

Cancer stem cells in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is one of the most intractable challenges among human diseases with poor prognosis and shortness of effective therapeutic options. Cancer stem cells (CSCs), a tumor sub-population, are considered the cause of tumor growth, differentiation, metastasis and therapeutic resistance, etc. In this review, we discuss the known methods for isolation and verification of ESCC CSCs, the biomarkers of ESCC CSCs and their significance in diagnosis and prognosis. Then we review the ESCC CSC signaling pathway and therapeutic resistance. In pace with the detailed studies of ESCC CSCs increasing, treatment strategies of ESCC based on CSCs are becoming more promising.

U-Shaped Relationship of Non-HDL Cholesterol With All-Cause and Cardiovascular Mortality in Men Without Statin Therapy.

Background: Non-HDL-C is well established causal risk factor for the progression of atherosclerotic cardiovascular disease. However, there remains a controversial pattern of how non-HDL-C relates to all-cause and cardiovascular mortality, and the concentration of non-HDL-C where the risk of mortality is lowest is not defined. Methods: A population-based cohort study using data from the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2014. Male participants without statin therapy were divided into the six groups according to non-HDL-C levels (<100, 100-129, 130-159, 160-189, 190-219, ≥220 mg/dl). Multivariable Cox proportional hazards models were conducted with a hazard ratio (HR) and corresponding 95% confidence interval (CI). To further explore the relationship between non-HDL-C and mortality, Kaplan-Meier survival curves, restricted cubic spline curves, and subgroup analysis were performed. Results: Among 12,574 individuals (average age 44.29 ± 16.37 years), 1,174(9.34%) deaths during a median follow-up 98.38 months. Both low and high non-HDL-C levels were significantly associated with increased risk of all-cause and cardiovascular mortality, indicating a U-shaped association. Threshold values were detected at 144 mg/dl for all-cause mortality and 142 mg/dl for cardiovascular mortality. Below the threshold, per 30 mg/dl increase in non-HDL-C reduced a 28 and 40% increased risk of all-cause (p < 0.0001) and cardiovascular mortality (p = 0.0037), respectively. Inversely, above the threshold, per 30 mg/dl increase in non-HDL-C accelerated risk of both all-cause mortality (HR 1.11, 95% CI 1.03-1.20, p = 0.0057) and cardiovascular mortality (HR 1.30, 95% CI 1.09-1.54, p = 0.0028). Conclusions: Non-HDL-C was U-shaped related to all-cause and cardiovascular mortality among men without statin therapy.

Associations Between Serum Soluble α-Klotho and the Prevalence of Specific Cardiovascular Disease.

Objective: Accumulating experimental evidence has identified the beneficial effects of the anti-aging protein, serum soluble α-Klotho, on longevity, and the cardiovascular system. Although a previous study has revealed the predictive value of α-Klotho on total cardiovascular disease (CVD), the associations between α-Klotho and specific CVDs, including congestive heart failure (CHF), coronary heart disease (CHD), myocardial infarction (MI), and stroke, remains to be fully elucidated in humans. Methods: For 8,615 adults in the 2007 to 2016 National Health and Nutrition Examination Survey, stratified multivariable logistic regression models, restricted cubic spline curves, and subgroup analyses were used to evaluate the associations between α-Klotho and the four specific CVDs. Results: In the quartile analyses, compared to those in the highest quartile, participants in the lowest level of α-Klotho were significantly associated with CHF [odds ratio (OR) = 1.46, 95% CI: 1.09-1.97] and MI (1.33, 1.02-1.74), which was not the case for CHD (1.12, 0.91-1.38) or stroke (0.96, 0.73-1.25). Each unit increment in the ln-transformed α-Klotho concentrations was only positively associated with a 38 and 24% reduction in the prevalence of CHF and MI, respectively. Restricted cubic spline curves indicated that the α-Klotho was correlated with CHF and MI in linear-inverse relationships. Conclusion: The present findings suggested that the serum soluble α-Klotho is significantly associated with the prevalence of CHF and MI. To better determine whether α-Klotho is a specific biomarker of CVD, particularly for CHD and stroke, further research in humans is needed.