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Cancer stem cells (CSCs) are considered key contributors to tumor progression, and ferroptosis has been identified as a potential target for CSCs. We have previously shown that butyrate enhances the ferroptosis induced by erastin in lung cancer cell, this study aimed to investigate the impact of butyrate on the progression of lung CSCs. To investigate these effects, we constructed a series of in vitro experiments, including 3D non-adherent sphere-formation, cytometry analysis, assessment of CSC marker expression, cell migration assay, and in vivo tumorigenesis analyses. Additionally, the influence of butyrate on chemotherapeutic sensitivity were determined through both in vitro and in vivo experiments. Mechanistically, immunofluorescence analysis was employed to examine the localization of biotin-conjugated butyrate. We identified that butyrate predominantly localized in the lysosome and concurrently recruited Fe2+ in lysosome. Moreover, butyrate reduced the stability of SLC7A11 protein stability in lung cancer cells through ubiquitination and proteasome degradation. Importantly, the effects of butyrate on lung CSCs were found to be dependent on lysosome Fe2+- and SLC7A11-mediated ferroptosis. In summary, our results demonstrate that butyrate could induce the ferroptosis in lung CSCs by recruiting Fe2+ in lysosome and promoting the ubiquitination-lysosome degradation of SLC7A11 protein.

Herein, pyridinium and 4-vinylpyridinium groups are introduced into the VIE-active N,N′-disubstituted-dihydrodibenzo[a,c]phenazines (DPAC) framework to afford a series of D-π-A-structured dihydrodibenzo[a,c]phenazines in consideration of the aggregation-benefited performance of the DPAC module and the potential mitochondria-targeting capability of the resultant pyridinium-decorated DPACs (DPAC-PyPF6 and DPAC-D-PyPF6). To modulate the properties and elucidate the structure–property relationship, the corresponding pyridinyl/4-vinylpyridinyl-substituted DPACs, i.e., DPAC-Py and DPAC-D-Py, are designed and studied as controls. It is found that the strong intramolecular charge transfer (ICT) effect enables the effective separation of the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO) of DPAC-PyPF6 and DPAC-D-PyPF6, which is conducive to the generation of ROS. By adjusting the electron-accepting group and the π-bridge, the excitation, absorption, luminescence, photosensitizing properties as well as the mitochondria-targeting ability can be finely tuned. Both DPAC-PyPF6 and DPAC-D-PyPF6 display large Stokes shifts (70–222 nm), solvent-dependent absorptions and emissions, aggregation-induced emission (AIE), red fluorescence in the aggregated state (λem = 600–650 nm), aggregation-promoted photosensitizing ability with the relative singlet-oxygen quantum yields higher than 1.10, and a mitochondria-targeting ability with the Pearson coefficients larger than 0.85. DPAC-D-PyPF6 shows absorption maximum at a longer wavelength, slightly redder fluorescence and better photosensitivity as compared to DPAC-PyPF6, which consequently leads to the higher photocytotoxicity under the irradiation of white light as a result of the larger π-conjugation.

Abstract Background Intracardiac septal defect is repaired using median sternotomy in most centers; however, there are several reports using minimally invasive surgery in both children and adults. This study summarized our strategy of minimally invasive therapy using various lateral mini-thoracotomies in patients with congenital septal defect. Methods In this study, 472 patients who underwent minimally invasive repair of intracardiac septal defects (atrial septal defect, (ASD), ventricular septal defect, (VSD), and atrioventricular septal defect, (AVSD)) from January 2012 to June 2020 were retrospectively reviewed. Those who underwent device closure were excluded. The minimally invasive strategy included three groups: the right sub-axillary vertical incision (RSAVI) group (N = 335, including192 ASDs, 135 VSDs and 8 AVSDs); the right anterolateral thoracotomy (RALT) group (N = 132, including 77 ASDs, 51 VSDs and 4 AVSDs); and the left anterolateral thoracotomy (LALT) group (N = 5, all subpulmonary VSDs). Results Concomitant surgeries included nine cases of right ventricular outflow tract obstruction relief, nine cases of mitral repairs and 37 cases of tricuspid repairs. There was one transition from thoracotomy to sternotomy. Three patients required second pump run for residual lesions (two residual VSD shunts and one mitral regurgitation). The age and body weight of the RSAVI group were significantly lower than those of the RALT and LALT groups (all P

Tricuspid regurgitation (TR) may occur late after left-sided valve surgery (LSVS). Isolated tricuspid regurgitation after left-sided valve surgery (iTR-LSVS) refers to isolated TR without significant lesions in the mitral and/or aortic position late after mitral and/or aortic replacement or repair. Severe TR has a negative impact on long-term prognosis and requires surgical or transcatheter treatment. However, there is no clear recommendation on when and how intervention should be performed for patients with iTR-LSVS in the current guidelines for the management of valvular heart disease. The historically high operative mortality may be reduced by current minimally invasive techniques and transcatheter therapy. To further understand iTR-LSVS, standardize the treatment, improve the prognosis, and promote the collaboration, the Chinese Minimally Invasive Cardiovascular Surgery Committee (CMICS) wrote this expert consensus on the management of iTR-LSVS from the aspects of etiology, preoperative evaluation, indications for intervention, surgical treatment, transcatheter therapy, and postoperative management.

Lung cancer: Targeting a vicious circle Therapies targeting a molecular feedback loop involved in tumor growth may prove valuable for treating non-small-cell lung cancer. Fangbao Ding, Jianbing Huang, and co-workers at Shanghai Jiao Tong University in Shanghai, China, have shown how an enzyme called USP21 promotes cancer cell proliferation and tumor growth in non-small-cell lung cancer. The team took cancerous and non-cancerous lung tissue samples from 42 patients, and analyzed the expression and behavior of USP21. The enzyme was highly expressed in cancerous tissues, where it stabilized a known gene with the potential to cause cancer called YY1. This gene also regulated the expression of a particular RNA molecule, which in turn worked to increase levels of USP21. This cyclical process encouraged the proliferation, migration and invasion of non-small-cell lung cancer cells, and may provide a future therapeutic target.

Abstract Background Primary cardiac tumors are rare and the majorities are benign. Conventional surgical treatment uses median sternotomy, while minimally invasive surgery from right anterolateral minithoracotomy has become an alternative method in recent years. In this study, we summarized the surgical outcomes of both approaches. Methods From January 2008 to August 2018, 50 patients with primary benign cardiac tumors underwent either conventional or minimally invasive surgery in our department. The baseline data were collected. The peri-operative data and follow up results were compared between the two groups. Results There were19 men and 31 women enrolled in this study with a mean age of 55.0 ± 17.5 years. The most common site of the tumor was left atrium (n = 40, 80%), followed by right atrium (n = 8, 16.0%), right ventricle (n = 1, 2.0%) and left ventricle (n = 1, 2.0%). All patients underwent surgery uneventfully, including 33 cases (66.0%) of median sternotomy and 17 cases (34.0%) of right anterolateral minithoracotomy. No significant differences were found between the two groups in terms of cardiopulmonary bypass time, aortic cross-clamp time, postoperative intubation time, intensive care unit days and length of the hospital stay. Patients with right anterolateral minithoracotomy had less post-operative chest drainage (536 ± 159 vs 773 ± 255 ml, P

Currently, fossil fuels such as oil, coal, and natural gas are the world's primary energy sources. However, it is anticipated that these energy sources will be depleted in less than 100 years. As such, the development of new energy technologies is urgently needed. Biomass is one of the earliest sources of energy, and is used especially in rural areas where it is often the only one that is accessible and affordable. With the depletion of fossil fuels and increasing environmental degradation, biomass energy is attracting increasing attention around the world. Compared with fossil fuel, biomass is carbon neutral and sustainable, and has a smaller greenhouse gas footprint and lower SO2 emission levels. In addition, biomass energy remains the only renewable green energy that can be stored and transported. A number of countries have developed mature and proven combustion technologies, but these technologies are mainly based on wood biomass fuels. Unlike these developed countries, China is a large agricultural country with a limited amount of available firewood. As such, foreign experience cannot be fully applied in China. Although biomass fuels typically have relatively low fuel-N contents, this fuel-N between 70%-100% mass fraction is converted to NOx during combustion. In addition, the combustion of straw and other biomass fuels emits more NOx than wood fuels. In recent years, the air quality in China has become a serious public health concern, and NOx is a widespread atmospheric pollutant with significant impacts on human health and the economy. In this paper, an overview of biomass combustion technologies and NOx control systems in China and around the world was presented, and their advantages and disadvantages were summarized. The main bottleneck was identified in NOx control technologies with respect to biomass boilers in China and the development of new technologies in this field was predicted.

Objective. The purpose is to observe the effects and neural mechanism of cutting upper thoracic sympathetic trunk (TST) on the ventricular rate (VR) during persistent atrial fibrillation (AF). Methods. Twelve beagle dogs were halving to the control group and experimental group, 6 dogs for each group. Both groups were performed with left atrial rapid pacing (600 beats/min) to induce sustained AF. The experimental group underwent cutting upper TST after a sustained AF model was established, while the control group received thoracotomy without cutting TST. Bilateral stellate ganglion (SG) and left atrial myocardium were harvested for tyrosine-hydroxylase (TH) immunohistochemical staining. Results. After cutting upper TST for 30 minutes, the average VR was 121.5 ± 8.7 bpm (95% CI, 114.8 to 128.0) in the experimental group, which was significantly slower than that of the control group (144.5 ± 4.2 bpm (95% CI, 141.5 to 148.0)) (P

Epithelial mesenchymal transition (EMT) is a critical step in cancer metastasis. Some evidences have been provided to verify up-regulation of linc00511 in multiple cancers and oncogenic roles during cancer malignant process. But, the roles of linc00511 on the metastasis of lung cancer are still largely unclear. Our study aims to reveal the functional effects of linc00511 on TGF-β1-induced EMT in lung cancer. Our results showed that knockdown of linc00511 significantly inhibited TGF-β1-induced migration and invasion and down-regulated the mRNA and protein levels of MMP2, MMP9 and MMP12 in TGF-β1 treated SPCA1 and H1975 cells. Also, western blotting results showed that inhibition of linc00511 remarkably suppressed TGF-β1-induced N-cadherin, Vimentin and snail and increased E-cadherin expression in SPCA1 and H1975 cells. Noteworthy, we further found that inhibition of linc00511 could down-regulate TGF-β1-induced ZEB2 mRNA and protein levels by sponging miR-183-5p in SPCA1 and H1975 cells. Taken together, our findings suggested knockdown linc00511 suppressed TGF-β1-induced migration and invasion via inhibiting EMT and MMPs in lung cancer cells.

The difficulty in recovering the aggregation-induced emission fluorogens (AIEgens) to the initial dispersed state upon illuminating has limited their applications. Here, the authors employ the confined space in the quartz nanopore to achieve a nanopore-size dependent restriction of AIEgens.

Background/Aims: Pulmonary fibrosis is a common outcome of various interstitial lung diseases. Prodigiosin (PG) is a series of red pigment with methoxypyrrole ring. This studyinvestigates therole of prodigiosin in pulmonary fibrosis and its underlying mechanisms. Methods: A pulmonary fibrosis rat model was established by intra-trachealinjection ofbleomycin A5. Rats were divided into 4 groups: Normal group, pulmonary fibrosis Model group, Prodigiosin treatment group and hydrocortisone treatmentgroup. HE and Masson staining were carried outto evaluate histopathological changes. The content of hydroxyproline in lung tissue was determined by alkaline hydrolysis. The expression of PICP and PIIINP was examined by ELISA. The mRNA expression of miR-410, TGF-β1 and ADAMTS1 in lung homogenate were detected by RT-PCR. The bronchoalveolar lavage fluid (BALF) and lung tissues of rats were collected and analyzed. Human embryonic pulmonary fibroblast (HEPF) was used for study in vitro. A dual-luciferase reporter assay was conducted to examine the effect of miR-410 on ADAMTS1 expression. Cell transfection was conducted to inhibit miR-410. MTT assay was performed to investigate cell proliferation. The expressions of miR-410, TGF-β1, ADAMTS1and other fibrosis related biomarkers (Col I, Col III, and α-SMA) wereexamined by RT-PCR and Western Blot. Results: HE and Masson staining showed thickened alveolar septum, hyperplasticcapillaries, and large areas of collagen fiber deposition in pulmonary fibrosis model rats. Rats in prodigiosin and hydrocortisone treatment groups had alleviated symptoms. There was high hydroxyproline expression in model rats, whereas the expression of hydroxyproline reduced after prodigiosin or hydrocortisone treatments. RT-PCR results showed high miR-410,high TGF-β1 and low ADAMTS1 in lung tissue of model rats. The expression of PICP and PIIINP werehigher in BALF of model group than in treatment groups. Prodigiosin and hydrocortisone treatment significantly reduced PICP and PIIINP content. RT-PCR and Western Blot analysis showed that prodigiosin inhibited expression of miR-410 and TGF-β1, but up-regulated ADAMTS1 expression. MTT assay indicated that prodigiosin inhibited HEPF proliferation induced by miR-410 overexpression. Conclusion: Prodigiosin down-regulates the expression of miR-410 and TGF-β1, up-regulates ADAMTS1, leading to decrease accumulation of fibrotic proteins. It could be used in alleviating pulmonary fibrosis.

Abstract To investigate roaming paths planning for diagnosis of congenital heart diseases (CHD) using a cardiovascular virtual endoscopy (VE) system. Forty children were enrolled. VE system was applied to support in establishing a diagnosis. Performance in diagnosing CHDs by CT, VE using automatically planned roaming paths (VE-auto, objects were treated as left heart system and right heart system), VE using manually planned paths (VE-manual), and VE using automatically planned path for left heart system and manually planned path for right heart system (VE-combined) were studied and compared. Comparable accuracy of 93%, 93%, 95% and 95% was found by CT, VE-auto, VE-manual and VE-combined. However, in diagnosing tetralogy of Fallot, significantly higher performance was found by VEs, compared with CT. For VE-auto, poor performance with an accuracy of 85% and sensitivity of 22% was revealed in diagnosing muscular ventricular septal defect, compared with VE-manual and VE-combined. Compared with VE-manual, VE-combined illustrated comparable diagnostic accuracy on all CHDs; however, significantly smaller diagnostic time was utilized (P

Background/Aims: Neointimal formation following vascular injury remains a major mechanism of restenosis, whereas the precise sources of neointimal cells are still uncertain. We tested the hypothesis that both injured arterial cells and non-arterial cells contribute to intimal hyperplasia. Methods: Following allograft transplantation of the balloon-injured carotid common artery (n = 3-6), the cellular composition of the transplant grafts and the origins of neointimal cells were measured by immunohistochemistry and immunofluorescence staining. Results: Smooth muscle actin (SMA)-positive and CD68-positive cells were clearly observed 14 days later in the neointima after allograft transplantation of the balloon-injured carotid common artery, where re-endothelialization was not yet complete. Green fluorescent protein (GFP) and wild-type (WT) allograft transplantation revealed that the majority of the neointima cells were apparently from the recipient (≈85%) versus the donor (≈15%). Both monocyte chemotactic protein-1 (MCP-1)/CCR2 and stromal cell-derived factor-1 (SDF-1)/CXCR4 signaling were involved in intimal hyperplasia, with bone marrow-derived cells also playing a role. Conclusion: These data support the hypothesis that intimal hyperplasia could develop in our novel rat allograft transplantation model of arterial injury, where neointima is attributable not only to local arterial cells but also non-arterial cells including the bone marrow.

Non-small cell lung cancer (NSCLC) is one of the causes of cancer mortality worldwide. The role of miR-26 in the development and progression of NSCLC remains largely unknown. In this study we found an abnormal expression of miR-26 in human NSCLC tissues. It was found that miR-26 mimics induced cell apoptosis and promoted caspase-3, 9 activities in human NSCLC cells. The miR-26 inhibitor enhanced the expression of the light chain 3 (LC3) protein and the autophagy related genes in NSCLC cells. Moreover, miR-26 regulated apoptosis and autophagy by inhibiting TGF-β expression in a JNK dependent manner. In addition, miR-26 mimics induced cell apoptosis, was involved in the endoplasmic reticulum stress (ERS) signaling pathway. Down-regulation of the ERS, inhibited apoptosis which was induced by miR-26 mimics in NSCLC cells. In in vivo studies, TUNEL staining revealed that the number of TUNEL positive cells of the tumor tissue in the miR-26 treatment group, were significantly increased in comparison with the control group, while the number of TUNEL positive cells in the tumor tissue were remarkably decreased in the groups treated with miR-26, combined with the TGF-β1 inhibitor or JNK inhibitor. Additionally, the immunoreactivity of TGF-β1 in the cells treated with the miR-26 inhibitor, decreased in comparison to the control group. Our results indicated that miR-26 induced apoptosis and inhibited autophagy in human NSCLC cells through the TGF-β1-JNK signaling pathway, suggesting that miR-26 could be a potential novel target for the treatment of NSCLC.

Background: Right minithoracotomy (RM) has been proven to be a safe and effective approach for mitral valve surgery, but the differences of artificial chordae technique between RM and median sternotomy (MS) were seldom reported. Here, we compared the outcomes of modified artificial chordae technique for mitral regurgitation (MR) through RM or MS approaches. Methods: One hundred and eighteen consecutive adult patients who received mitral valve repair with artificial chordae and annuloplasty for MR through RM (n = 58) or MS (n = 60) from January 2006 to January 2015 were analyzed. Results: All of the selected patients underwent mitral valve repair successfully without any complication during the surgery. There was no significant difference between RM group and MS group in cardiopulmonary bypass time, aortic cross-clamp time, and early postoperative complications. However, compared with the MS group, the RM group had shorter hospital stay and faster surgical recovery. At a mean follow-up of 44.8 ± 25.0 months, the freedom from more than moderate MR was 93.9% ± 3.5% in RM group and 94.8% ± 2.9% in MS group at 3 years postoperatively. Log-rank test showed that there was no significant difference in the freedom from recurrent significant MR between the two groups (χ2 = 0.247, P = 0.619). Multivariate analysis revealed that the presence of mild MR at discharge was the independent risk factor for the recurrent significant MR. Conclusion: Right minithoracotomy can achieve the similar therapeutic effects with MS for the patients who received modified artificial chordae technique for treating MR.

Introduction. Catheter-based renal denervation (RDN) could reduce cardiac sympathetic nerve activity (SNA) and inhibit atrial fibrillation (AF). However, the reliability is uncertain, because the renal sympathetic nerves are mainly distributed in the adventitial surface of the renal artery. Objective. The aims of this study were to test the hypothesis that renal artery adventitial ablation (RAAA) definitely had the effects of RDN and to study the effects of RDN via renal artery adventitial cryoablation (RAAC) on AF and cardiac neural remodeling. Methods. Twenty beagle canines were randomly assigned to two groups: the left RDN group (LRDN, n=10), which underwent left RDN via RAAC; the Sham group (n=10). After 2 months of postoperative recovery, AF vulnerability, AF duration, and histological examination were performed in both groups. Results. Compared with the Sham group, left stellate ganglion (LSG) tissue fibrosis was increased in the LRDN group. LRDN significantly increased the percentage of TH-negative ganglionic cells and decreased the density of TH-positive nerves in the LSG (P

Increasing evidence suggests that ubiquitin-specific protease 22 (USP22) has great clinicopathologic significance in oncology. In this study, we investigated the role of USP22 in human NSCLC tumorigenesis along with the underlying mechanisms of action. First, we determined the expression of USP22 in human NSCLC, as well as normal tissues and cell lines. We then studied the effects of USP22 silencing by shRNA on NSCLC cell growth in vitro and tumorigenesis in vivo, along with the effect on the p53 pathway. We found that USP22 is overexpressed in human NSCLC tissues and cell lines. USP22 silencing by shRNA inhibits proliferation, induces apoptosis and arrests cells at the G0/G1 phases in NSCLC cells and curbs human NSCLC tumor growth in a mouse xenograft model. Additionally, USP22 silencing downregulates MDMX protein expression and activates the p53 pathway. Our co-immunoprecipitation analysis shows that USP22 interacts with MDMX in NSCLC cells. Furthermore, MDMX silencing leads to growth arrest and apoptosis in NSCLC cells, and over-expression of MDMX reverses the USP22 silencing-induced effects. Taken together, our results suggest that USP22 promotes NSCLC tumorigenesis in vitro and in vivo through MDMX upregulation and subsequent p53 inhibition. USP22 may represent a novel target for NSCLC treatment.

Background/Aims: Most cardiac procedures involve the use of cardiopulmonary bypass (CPB), which pumps oxygenated blood to the body while the heart and lungs are isolated. CPB can cause profound alterations V in the homeostasis of physiological fluids, which often results in myocardial edema. In our study, we used sheep CPB model of in vivo and in vitro to assess the relationship between cGMP and AQP1 during CPB. Methods: ODQ, a specific inhibitor of soluble guanylate cyclase (sGC), was used to treat the CPB animals or cardiomyocytes. Left ventricular function of each group was determined by pressure-volume system. Water content of myocardial tissue was assessed by dry-wet weight, and cardiomyocytes water permeability was also calculated. The concentration of cGMP was determined by Radioimmunoassay (RIA). mRNA and protein expression of AQP1 were detected by real-time PCR and western blot, respectively. Results: The relative expression level of AQP1 mRNA and protein at each time point (0, 6, 12, 24 or 48 h) after CPB was significantly increased (1.18-fold at 12 h, 1.77-fold at 24 h and 2.18-fold at 48h) compared with each sham group, the protein expression of AQP1 also showed a rising trend after CPB. The degree of myocardial edema (75.1% at 12 h, 79.3% at 24 h and 81.0% at 48h) increased following the CPB surgery. The mRNA expression level of AQP1 was significantly decreased by 39.7% (pin vitro experiments showed the same changing trends as in vivo. Conclusion: cGMP pathway controls water channels and then affects water intake during CPB through an AQP1-mediated pathway.

Mg alloy is the preferred material for the lightweight development of manufacturing industry. However, its application is limited due to the poor wear resistance and corrosion resistance. In this experiment, Mg–Al layered double hydroxide/steam coating (LDH/SC) composite coatings are prepared on the surface of LA43M Mg–Li alloy by steam treatment and in‐situ hydrothermal method for different times (12, 18, 24, 30, and 36 h). The morphology and structure of the coatings are characterized by scanning electron microscopy, energy dispersive spectrometry, and X‐ray diffractometer, and the friction wear test of the coatings is carried out. The corrosion resistance of the coatings is evaluated by immersion tests and hydrogen evolution experiments. The effect of hydrothermal time on the growth characteristics, wear resistance, and corrosion behavior of LDH/SC coatings in 3.5 wt% NaCl solution is systematically investigated. In addition, the growth mechanism and corrosion resistance mechanism of the LDH/SC coating are discussed. The results show that the composite coatings is mainly composed of LDH and Mg(OH)2 phases. Appropriately prolonging the hydrothermal reaction time is beneficial to the nucleation and growth of LDH. When the hydrothermal time is 30 h, the prepared coating has the best density, and the prepared coating can significantly improve the corrosion resistance and friction wear properties of the substrate. [ABSTRACT FROM AUTHOR]

Background: In previous studies, the 308‐nm light‐emitting diode (LED) has been proven safe and effective for treating vitiligo. However, direct comparisons between the 308‐nm LED and 308‐nm excimer lamp (308‐nm MEL) for the treatment of vitiligo are lacking. Objective: To compare the efficacy of the 308‐nm LED and 308‐nm MEL for treating nonsegmental stable vitiligo. Patients and Methods: This randomized controlled trial was conducted between January 2018 and August 2023. Enrolled patients were randomly assigned to either the 308‐nm LED or the 308‐nm MEL groups, both receiving 16 treatment sessions. Adverse events that occurred during the treatment were documented. Results: In total, 269 stable vitiligo patches from 174 patients completed the study. A total of 131 lesions were included in the 308‐nm LED group, and 138 lesions were included in the 308‐nm MEL group. After 16 treatment sessions, 38.17% of the vitiligo patches in the 308‐nm LED group achieved repigmentation of at least 50% versus 38.41% in the 308‐nm MEL group. The two devices exhibited similar results in terms of efficacy for a repigmentation of at least 50% (p =.968). The incidence of adverse effects with the two phototherapy devices was comparable (p =.522). Conclusions: Treatment of vitiligo with the 308‐nm LED had a similar efficacy rate to the 308‐nm MEL, and the incidence of adverse effects was comparable between the two devices. [ABSTRACT FROM AUTHOR]