Suspended Micro/Nanofiber Hierarchical Biological Scaffolds Fabricated Using Non-Electrospinning STEP Technique

Extracellular matrix (ECM) is a fibrous natural cell environment, possessing complicated micro- and nanoarchitectures, which provide extracellular signaling cues and influence cell behaviors. Mimicking this three-dimensional microenvironment in vitro is a challenge in developmental and disease biology. Here, suspended multilayer hierarchical nanofiber assemblies (diameter from micrometers to less than 100 nm) with accurately controlled fiber orientation and spacing are demonstrated as biological scaffolds fabricated using the non-electrospinning STEP (Spinneret based Tunable Engineered Parameter) fiber manufacturing technique. Micro/nanofiber arrays were manufactured with high parallelism (relative angles between fibers were maintained less than 6°) and well controlled interfiber spacing (<15%). Using these controls, we demonstrate a bottom up hierarchical assembly of suspended six layer structures of progressively reduced diameters and spacing from several polymer systems. We then demonstrate use of STEP scaffolds to study single and multicell arrangement at high magnifications. Specifically, using double layer divergent (0°–90°) suspended nanofibers assemblies, we show precise quantitative control of cell geometry (change in shape index from 0.15 to 0.57 at similar cell areas), and through design of scaffold porosity (80 × 80 μm² to 5 × 5 μm²) quadruple the cell attachment density. Furthermore, using unidirectional or crisscross patterns of sparse and dense fiber arrays, we are able to control the cell spread area from ∼400 to ∼700 μm², while the nucleus shape index increases from 0.75 to 0.99 with cells nearly doubling their focal adhesion cluster lengths (∼15 μm) on widely spaced nanofiber arrays. The platform developed in this study allows a wide parametric investigation of biophysical cues which influence cell behaviors with implications in tissue engineering, developmental biology, and disease biology

Table_1_Preparation and characterization of chitosan/whey isolate protein active film containing TiO2 and white pepper essential oil.DOCX

Active packaging films are designed to improve quality and extend the food shelf life by incorporating functional active ingredients into biopolymer films. This study developed a bioactive film based on chitosan (CS) and whey isolated protein (WPI) incorporated with 0.01 wt% TiO2 and 0.1 wt% white pepper essential oil (WPEO). The physicochemical properties of the prepared film were also evaluated comprehensively. The results showed that water solubility and water vapor permeability of the film incorporated with TiO2 and WPEO were 25.09% and 0.0933 g mm m–2 h–1 KPa–1, respectively, which were significantly higher than those of other films (P 2 and WPEO have improved. The films were characterized by Fourier transform infrared (FTIR) and scanning electron microscopy (SEM). The FTIR results showed interactions between TiO2 and WPEO with CS/WPI compound, and the SEM results indicated a good incorporation of TiO2 into the composite films. The antioxidative and antibacterial properties of films were significantly enhanced by incorporating WPEO. According to results, the developed biocomposite film can be considered as a packaging material.</p

Facile Synthesis of Amorphous MnO_x Catalysts for Efficient Ozone Elimination in Domestic Refrigerators

Amorphous manganese oxide catalysts, aimed at efficient ozone removal in refrigerators, were synthesized using a simple redox method. Factors like crystallinity of structure, textural properties, and Fe doping significantly affect the catalyst’s performance. The Fe-doped KMF-250 showcased outstanding ozone decomposition capabilities, efficiently eliminating 10,000 ppb of ozone at an average rate of ca. 13.3 , under conditions of 6 °C and 36% relative humidity in a refrigerator chamber (144 L). Moreover, this catalyst exhibits extraordinary stability, outperforming existing commercial catalysts in terms of both durability and efficiency. The incorporation of even a minimal amount of Fe (0.84 wt%) considerably raised the amount of low-valence Mn, resulting in more crystal defects and oxygen vacancies. The existence of Fe in MnOx was also found playing an important role in promoting the desorption of the oxygen species and enhancing the oxygen mobility to generate oxygen vacancies, both of which contribute to the quick recovery of the catalyst. The catalyst’s large specific surface area, combined with optimal Fe doping, are crucial for its superior catalytic performance. This research delivers a potent MnOx catalyst suitable for ozone removal in refrigerators and viable for mass production.</p

Additional file 4: of Quality assessment of systematic reviews on total hip or knee arthroplasty using mod-AMSTAR

Appendix 4. Data extraction table: Extraction items and results of each study. (Data extraction table). (XLSX 21 kb

Additional file 3: of Quality assessment of systematic reviews on total hip or knee arthroplasty using mod-AMSTAR

Appendix 3. AMSTAR score and list of included reviews: mod-AMSTAR score for each study and reference information of all included studies. (AMSTAR score and list of included reviews). (DOCX 58 kb

Additional file 1: of Quality assessment of systematic reviews on total hip or knee arthroplasty using mod-AMSTAR

Appendix 1. Protocol: the protocol of this study. (Protocol). (DOCX 27 kb

Hepatitis C virus core protein activates autophagy through EIF2AK3 and ATF6 UPR pathway-mediated MAP1LC3B and ATG12 expression

<div><p>HCV infection induces autophagy, but how this occurs is unclear. Here, we report the induction of autophagy by the structural HCV core protein and subsequent endoplasmic reticular (ER) stress in Huh7 hepatoma cells. During ER stress, both the EIF2AK3 and ATF6 pathways of the unfolded protein response (UPR) were activated by HCV core protein. Then, these pathways upregulated transcription factors ATF4 and DDIT3. The ERN1-XBP1 pathway was not activated. Through ATF4 in the EIF2AK3 pathway, the autophagy gene ATG12 was upregulated. DDIT3 upregulated the transcription of autophagy gene <i>MAP1LC3B</i> (<i>LC3B</i>) by directly binding to the –253 to –99 base region of the <i>LC3B</i> promoter, contributing to the development of autophagy. Collectively, these data suggest not only a novel role for the HCV core protein in autophagy but also offer new insight into detailed molecular mechanisms with respect to HCV-induced autophagy, specifically how downstream UPR molecules regulate key autophagic gene expression.</p></div

Enhanced efficacy of curcumin with phosphatidylserine-decorated nanoparticles in the treatment of hepatic fibrosis

<p>Hepatic macrophages have been considered as a therapeutic target for liver fibrosis treatment, and phosphatidylserine (PS)-containing nanoparticles are commonly used to mimic apoptotic cells that can specifically regulate macrophage functions, resulting in anti-inflammatory effects. This study was designed to test the efficacy of PS-modified nanostructured lipid carriers (mNLCs) containing curcumin (Cur) (Cur-mNLCs) in the treatment of liver fibrosis in a rat model. Carbon tetrachloride-induced liver fibrosis in rats was used as an experimental model, and the severity of the disease was examined by both biochemical and histological methods. Here, we showed that mNLCs were spherical nanoparticles with decreased negative zeta potentials due to PS decoration, and significantly increased both mean residence time and area under the curve of Cur. In the rats with liver fibrosis, PS-modification of NLCs enhanced the nanoparticles targeting to the diseased liver, which was evidenced by their highest accumulation in the liver. As compared to all the controls, Cur-mNLCs were significantly more effective at reducing the liver damage and fibrosis, which were indicated by in Cur-mNLCs-treated rats the least increase in liver enzymes and pro-inflammatory cytokines in the circulation, along with the least increase in collagen fibers and alpha smooth muscle actin and the most increased hepatocyte growth factors (HGF) and matrix metalloprotease (MMP) two in the livers. In conclusion, PS-modified NLCs nanoparticles prolonged the retention time of Cur, and enhanced its bioavailability and delivery efficiency to the livers, resulting in reduced liver fibrosis and up-regulating hepatic expression of HGF and MMP-2.</p

Hyperuricemia and Risk of Incident Hypertension: A Systematic Review and Meta-Analysis of Observational Studies

<div><p>Background</p><p>Observational studies of the relationship between hyperuricemia and the incidence of hypertension are controversial. We conducted a systematic review and meta-analysis to assess the association and consistency between uric acid levels and the risk of hypertension development.</p><p>Methods</p><p>We searched MEDLINE, EMBASE, CBM (Chinese Biomedicine Database) through September 2013 and reference lists of retrieved studies to identify cohort studies and nested case-control studies with uric acid levels as exposure and incident hypertension as outcome variables. Two reviewers independently extracted data and assessed study quality using Newcastle-Ottawa Scale. Extracted information included study design, population, definition of hyperuricemia and hypertension, number of incident hypertension, effect sizes, and adjusted confounders. Pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) for the association between hyperuricemia and risk of hypertension were calculated using a random-effects model.</p><p>Results</p><p>We included 25 studies with 97,824 participants assessing the association between uric acid and incident hypertension in our meta-analysis. The quality of included studies is moderate to high. Random-effects meta-analysis showed that hyperuricemia was associated with a higher risk of incident hypertension, regardless of whether the effect size was adjusted or not, whether the data were categorical or continuous as 1 SD/1 mg/dl increase in uric acid level (unadjusted: RR = 1.73, 95% CI 1.46∼2.06 for categorical data, RR = 1.22, 95% CI 1.03∼1.45 for a 1 SD increase; adjusted: RR = 1.48, 95% CI 1.33∼1.65 for categorical data, RR = 1.15, 95% CI 1.06∼1.26 for a 1 mg/dl increase), and the risk is consistent in subgroup analyses and have a dose-response relationship.</p><p>Conclusions</p><p>Hyperuricemia may modestly increase the risk of hypertension incidence, consistent with a dose-response relationship.</p></div

Table1_Methylation-driven mechanisms of allergic rhinitis during pollen and non-pollen seasons using integrated bioinformatics analysis.xlsx

Background:Allergic rhinitis (AR) is a widespread allergic airway disease that results from a complex interplay between genetic and environmental factors and affects approximately 10%–40% of the global population. Pollen is a common allergen, and exposure to pollen can cause epigenetic changes. However, the mechanism underlying pollen-induced DNA methylation changes and their potential effects on the allergic march are still unclear. The purpose of this study was to explore the methylation-driven mechanisms of AR during the pollen and non-pollen seasons using bioinformatics analysis and to investigate their relationship with asthma.Methods:We downloaded DNA methylation and gene expression data from the GEO database (GSE50387: GSE50222, GSE50101) and identified differentially methylated positions (DMPs) and differentially expressed genes (DEGs) during the pollen and non-pollen seasons using the CHAMP and limma packages. Through correlation analysis, we identified methylation-driven genes and performed pathway enrichment analysis to annotate their functions. We incorporated external data on AR combined with asthma (GSE101720) for analysis to identify key CpGs that promote the transformation of AR to asthma. We also utilized external data on olive pollen allergy (GSE54522) for analysis to validate the methylation-driven genes. Weighted correlation network analysis (WGCNA) was employed to identify gene modules significantly correlated with pollen allergy. We extracted genes related to the key methylation-driven gene ZNF667-AS1 from the significant module and performed pathway intelligent clustering using KOBAS-i. We also utilized gene set enrichment analysis to explore the potential function of ZNF667-AS1.Results:We identified 20 and 24 CpG-Gene pairings during the pollen and non-pollen seasons. After incorporating external data from GSE101720, we found that ZNF667-AS1 is a key gene that may facilitate the transformation of AR into asthma during the pollen season. This finding was further validated in another external dataset, GSE54522, which is associated with pollen allergy. WGCNA identified 17 modules, among which the blue module showed significant correlation with allergies. ZNF667-AS1 was located in the blue module. We performed pathway analysis on the genes correlated with ZNF667-AS1 extracted from the blue module and identified a prominent cluster of pathways in the KOBAS-i results, including Toll-like receptor (TLR) family, MyD88, MAPK, and oxidative stress. Gene set enrichment analysis around cg05508084 (paired with ZNF667-AS1) also indicated its potential involvement in initiating and modulating allergic inflammation from the perspective of TLR and MAPK signaling.Conclusion:We identified methylation-driven genes and their related pathways during the pollen and non-pollen seasons in patients with AR and identified key CpGs that promote the transformation of AR into asthma due to pollen exposure. This study provides new insights into the underlying molecular mechanisms of the transformation of AR to asthma.</p