Viscoelasticity­Controlled Relaxation in Wrinkling Surface for Multistage Time­Resolved Optical Information Encryption.

As counterfeit techniques continue to evolve, ensuring the security of conventional "static" encryption methods becomes increasingly challenging. Here, the viscoelasticity-controlled relaxation is introduced for the first time in a bilayer wrinkling system by regulating the density of hydrogen bond networks in polymer to construct a "dynamic" encryption material. The wrinkling surface can manipulate light during the dynamic relaxation process, exhibiting three stages with frosted glass, structural color, and mirror reflection. By regulating the viscoelasticity of skin layer through UV irradiation, the wavelength and the relaxation rate of the wrinkles can be controlled. As a result, dynamic wrinkling anti-counterfeiting patterns and time-resolved multistage information encryption are achieved. Crucially, the encryption material is developed as an anti-counterfeiting label for packing boxes in daily applications, allowing the encrypted information to be activated manually and identified by naked eyes, surpassing the existing time-resolved encryption materials in utilization potential. Besides, the dynamic hydrogen bond networks are extended to various dynamic interaction networks, demonstrating the versatility of the dynamic encryption strategy. This work not only provides an additional dimension for dynamic information encryption in daily practical use, but also offers theoretical guidance for the development of advanced optical anti-counterfeiting and smart display materials in the future.

Fine mapping of a major QTL, qKl-1BL controlling kernel length in common wheat.

KEY MESSAGE: A major stable QTL, qKl-1BL, for kernel length of wheat was narrowed down to a 2.04-Mb interval on chromosome 1BL; the candidate genes were predicated and the genetic effects on yield-related traits were characterized. As a key factor influencing kernel weight, wheat kernel shape is closely related to yield formation, and in turn affects both wheat processing quality and market value. Fine mapping of the major quantitative trait loci (QTL) for kernel shape could provide genetic resources and a theoretical basis for the genetic improvement of wheat yield-related traits. In this study, a major QTL for kernel length (KL) on 1BL, named qKl-1BL, was identified from the recombinant inbred lines (RIL) in multiple environments based on the genetic map and physical map, with 4.76-21.15% of the phenotypic variation explained. To fine map qKl-1BL, the map-based cloning strategy was used. By using developed InDel markers, the near-isogenic line (NIL) pairs and eight key recombinants were identified from a segregating population containing 3621 individuals derived from residual heterozygous lines (RHLs) self-crossing. In combination with phenotype identification, qKl-1BL was finely positioned into a 2.04-Mb interval, KN1B:698.15-700.19 Mb, with eight differentially expressed genes enriched at the key period of kernel elongation. Based on transcriptome analysis and functional annotation information, two candidate genes for qKl-1BL controlling kernel elongation were identified. Additionally, genetic effect analysis showed that the superior allele of qKl-1BL from Jing411 could increase KL, thousand kernel weight (TKW), and yield per plant (YPP) significantly, as well as kernel bulk density and stability time. Taken together, this study identified a QTL interval for controlling kernel length with two possible candidate genes, which provides an important basis for qKl-1BL cloning, functional analysis, and application in molecular breeding programs.

Protective effects of different anti­inflammatory drugs on tracheal stenosis following injury and potential mechanisms.

Tracheal stenosis following injury cannot be effectively treated. The current study compared the protective effects of different anti­inflammatory drugs on tracheal stenosis and investigated their possible mechanisms. Rabbit tracheal stenosis models following injury were constructed and confirmed using hematoxylin and eosin (H&E) staining. A total of 30 rabbits were divided into the control (CON), penicillin (PEN), erythromycin (ERY), budesonide (BUD) and PEN + ERY + BUD groups (n=6). Stenotic tracheal tissue, serum and bronchoalveolar lavage fluid (BALF) were collected 10 days after continuous treatment. Pathological changes in the tracheas were observed by H&E staining. Histone deacetylase 2 (HDAC2) expression in tracheal tissues was detected by immunofluorescence. Immunohistochemistry was performed to detect collagen I (Col­I) and collagen III (Col­III) levels in tracheal tissues. Transforming growth factor ß1 (TGF­ß1), vascular endothelial growth factor (VEGF) and interleukin 8 (IL­8) levels in serum and BALF samples were determined using ELISA kits. Western blotting detected HDAC2, IL­8, TGF­ß1 and VEGF levels in tracheal tissues. H&E staining demonstrated that tracheal epithelial hyperplasia and fibroblast proliferation in the ERY and PEN + ERY + BUD groups markedly improved compared with the CON group. Furthermore, in tracheal tissues, HDAC2 expression was significantly increased and IL­8, TGF­ß1, VEGF, Col­I and Col­III levels were significantly decreased in the ERY and PEN + ERY + BUD groups compared with the CON group. Additionally, the results for the PEN + ERY + BUD were more significant compared with the ERY group. In serum and BALF samples, IL­8, TGF­ß1 and VEGF levels in the ERY and PEN + ERY + BUD groups were significantly lower compared with the CON group, with the results of the PEN + ERY + BUD group being more significant compared with the ERY group. There were no significant differences between the PEN, BUD and CON groups. ERY inhibited tracheal granulation tissue proliferation and improved tracheal stenosis following injury and synergistic effects with PEN and BUD further enhanced these protective effects. The mechanism may involve HDAC2 upregulation and inhibition of local airway and systemic inflammatory responses.

Expression of histone deacetylase 2 in tracheal stenosis models and its relationship with tracheal granulation tissue proliferation.

The current treatments for benign tracheal stenosis are inefficient. The present study examined the expression of histone deacetylase 2 (HDAC2) in different tracheal stenosis models and explored its association with the proliferation of tracheal granulation tissue and its ability to constitute a potential therapy for tracheal stenosis. Animal tracheal stenosis models were established, as indicated by hematoxylin and eosin (H&E) staining. A total of 24 New Zealand White rabbits were randomly divided into control, erythromycin, budesonide and vorinostat groups. Stenotic tracheal tissues were collected on day 11 after drug administration for 10 days. The degree of tracheal stenosis in each group was calculated, and pathological alterations were observed using H&E staining. The mRNA expression of HDAC2, interleukin-8 (IL-8), transforming growth factor-ß1 (TGF-ß1) and vascular endothelial growth factor (VEGF) was examined via reverse transcription-quantitative PCR. The protein expression of HDAC2 was examined via immunofluorescence, while the expression of type I and type III collagen was assessed using immunohistochemistry. The results of the present study demonstrated that tracheal epithelial hyperplasia in the erythromycin group was improved, the degree of hyperplasia being the lowest among all groups, and tracheal stenosis was reduced compared with the control group. In the vorinostat group, tracheal epithelial tissue hyperplasia was aggravated and stenosis was increased. The HDAC2 mRNA and protein levels were increased and decreased in the erythromycin and vorinostat groups, respectively. In contrast, the IL-8 mRNA expression levels were decreased and increased in the erythromycin and vorinostat groups, respectively. TGF-ß1, VEGF, type I and type III collagen expression was decreased in the erythromycin group, while TGF-ß1, VEGF and type III collagen expression was increased in the vorinostat group. Compared with the control, the budesonide group did not exhibit any alterations in all of the indicators examined, including TGF-ß1, VEGF, IL-8, HDAC2 and collagen. Erythromycin treatment upregulated the expression of HDAC2, inhibited the inflammatory responses and reduced the proliferation of tracheal granulation tissue. In contrast, vorinostat treatment downregulated HDAC2 expression, promoted the inflammatory responses and increased the proliferation of tracheal granulation tissue. These results suggest that regulating HDAC2 may be used as a potential treatment for benign tracheal stenosis.

Nintedanib ameliorates tracheal stenosis by activating HDAC2 and suppressing IL-8 and VEGF in rabbit.

Acquired tracheal stenosis is a common disease occurring after endotracheal intubation or tracheotomy. Currently, surgery is the main option to treat the stenosis. This study investigated therapeutic effect and possible mechanism of nintedanib on tracheal stenosis. The rabbit models of tracheal stenosis were established and were administered with nintedanib and budesonide. The damage and repair of the tracheal tissue were determined using hematoxylin and eosin (HE) staining. The expression of histone deacetylase 2 (HDAC2), interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) was detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western Blot and immunofluorescence assay. The expression of collagens I and III was assayed immunohistochemically. Remarkable tracheal stenosis was observed after the trachea was brushed in the rabbit model. Compared with control, the stenosis was improved after nintedanib treatment. The mRNA of HDAC2 was increased and that of IL-8 and VEGF was decreased significantly in the tracheal tissue following nintedanib treatment. Western blot analysis showed that HDAC2 increased to the level similar to that of control while VEGF remained unchanged following nintedanib treatment. Budesonide treatment also resulted in increased HDAC2 expression and decreased IL-8 and VEGF expression. Immunofluorescence assays also showed an increased HDAC2 expression following nintedanib treatment. Collagens I and III decreased significantly after nintedanib treatment in the tracheal tissues of models. Therefore, it is concluded that nintedanib alleviates the acquired tracheal stenosis by activating HDAC2 expression and suppressing IL-8 and VEGF expression, and may offer new option to medical treatment for the disease.

Role of Erythromycin-Regulated Histone Deacetylase-2 in Benign Tracheal Stenosis.

Objective: This study aims to explore the role of erythromycin-regulated histone deacetylase-2 in benign tracheal stenosis. Methods: The rabbit model of tracheal stenosis was established. The rabbits were randomly divided into 8 groups. Histone deacetylase-2 (HDAC2) expression was detected by immunofluorescence. The expression of type I collagen and type III collagen was detected by immunohistochemical method. The expression of TGF-ß1, VEGF and IL-8 in serum and alveolar lavage fluid was detected by ELISA. The expression of HDAC2, TGF-ß1, VEGF and IL-8 in serum and alveolar lavage fluid was detected by ELISA. The expression of HDAC2, TGF. Results: In Erythromycin (ERY) group, ERY + Budesonide group, ERY + Vorinostat group and ERY + Budesonide + Vorinostat group, the degree of bronchial stenosis was alleviated, and the mucosal epithelium was still slightly proliferated. The effect of ERY combined with other drugs was more obvious. The HDAC2 protein expression increased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group and decreased significantly in Vorinostat group, the expression of collagen I and III decreased significantly in ERY group, ERY + Budesonide group and ERY + Budesonide + Vorinostat group (P < 0.05). The TGF-ß1, VEGF and IL-8 in serum and alveolar lavage fluid was detected by ELISA. The expression of HDAC2, TGF-P < 0.05). The TGF. Conclusions: Erythromycin inhibited inflammation and excessive proliferation of granulation tissue after tracheobronchial mucosal injury by up-regulating the expression of HDAC2, it promoted wound healing and alleviated tracheobronchial stenosis. When combined with budesonide, penicillin and other glucocorticoids and antibiotics, it had a good synergistic effect. However, vorinostat could attenuate erythromycin's effect by down-regulating the expression of HDAC2. It may have good clinical application prospects in the treatment of tracheal stenosis.

An NIR-light-responsive surface molecularly imprinted polymer for photoregulated drug release in aqueous solution through porcine tissue.

The application of photoresponsive surface molecularly imprinted polymers based on azobenzene is limited by the UV light source required and their poor water solubility. Reducing the phototoxicity and solvent toxicity of the polymers therefore presents a challenge. In this work, an NIR-light-responsive surface molecularly imprinted polymer was fabricated by atom transfer radical polymerization using up-conversion nanoparticles as the core, a hydrophilic green-light-responsive azobenzene derivative as the functional monomer, and a drug as the template. The up-conversion nanoparticles core emitted green fluorescence in the range of 520-550 nm upon NIR irradiation (980 nm, 5 W cm-2), which was absorbed by the azobenzene containing molecularly imprinted polymers layer on the up-conversion nanoparticles surface. This caused the azobenzene chromophores to undergo trans→cis isomerization in phosphate buffered solution (pH = 7.4), thus resulting in NIR-light-induced drug release. The up-conversion fluorescence spectra were used to study the interaction mechanism between the azobenzene monomer and NIR light. Compared with structural analogues of the template (antifebrin and phenacetin), the NIR-light-responsive surface molecularly imprinted polymer showed excellent specificity of recognition for the template drug (paracetamol). The maximum adsorption capacity of the NIR-light-responsive surface molecularly imprinted polymer for loading of paracetamol was 16.80 µmol g-1. The NIR-light-responsive surface molecularly imprinted polymer was applied for NIR-light-induced paracetamol release in phosphate buffered solution (pH = 7.4) through porcine tissue. This work demonstrates the potential of drug delivery systems based on molecularly imprinted polymers for application in deep tissue delivery.

[Therapeutic effects and mechanism of saikosaponin-d in mice with bleomycin-induced pulmonary fibrosis].

OBJECTIVE: To study the therapeutic effects and mechanism of saikosaponin-d (SSd) in mice with bleomycin (BLM)-induced pulmonary fibrosis. METHODS: According to the random number table, 180 mice were randomly divided into 5 groups. Four groups were pulmonary fibrosis models. Fibrosis model mice were established by intratracheal injection of bleomycin (5 mgxkg(-1)). They were BLM, DXM, SSd and SSd + DXM groups (n = 40 each). At 1 hour post-modeling, DXM, SSd and SSd + DXM groups were injected ip with dexamethasone (DXM, 5 mgxkg(-1)xd(-1), 0.1 ml), SSd (1.8 mgxkg(-1)xd(-1), 0.18 ml), DXM + SSd (0.28 ml) respectively qd until Day 28. BLM group was similarly dosed with normal saline. In addition, a normal control group (NC group, n = 20) treated likewise. The mice were anesthetized and sacrificed at Days 3, 7, 14, 28 for harvests of serum and lung tissue samples. The conventional histopathological changes of lung tissue were observed. Except for NC group, modeling groups of mice were used to observe the natural survival rate. Such indices as superoxide dismutase (SOD) and malonaldehyde (MDA) were examined both in lung tissue and serum samples. And hydroxyproline (HYP) was tested only in lung tissue. RESULTS: SSd could markedly increase the survival rate (80.0% in SSd and SSd + DXM groups vs 50.0% in BLM group, P < 0.05) and reduce alveolitis and fibrosis in mice. In comparison with BLM group, the levels of HYP of three treatment groups (DXM, SSd and SSd + DXM) in lung tissue was significantly lower (P < 0.05) at Days 14 and 28. The levels of MDA both in serum and lung tissue were significantly lower at Days 3, 7 and 14 (P < 0.05). The serum level of SOD was significantly higher at Days 3, 7 and 14 while the level of SOD in lung tissue was significantly higher at Days 3 and 7 (P < 0.05, P < 0.01). CONCLUSIONS: SSd has marked therapeutic effects upon bleomycin-induced pulmonary fibrosis in mice. And the mechanism may be associated with its anti-lipid peroxidation effect.