U-shaped association between serum calcium and in-hospital mortality in diabetes patients with congestive heart failure: a cohort study.

Previous studies have reported that the significant association between serum calcium and mortality substantially in patients, especially among those with intensive care unit (ICU). And In diabetes mellitus, congestive heart failure (CHF) is a significant comorbidity. We aim to evaluate the association between serum calcium levels and in-hospital mortality among patients with diabetes and congestive heart failure. The participants in this study were extracted from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. To scrutinize potential associations between serum calcium levels and in-hospital mortality, a comprehensive analysis encompassing multivariate logistic regression, cubic spline function model, threshold effect analysis, and subgroup analysis was performed. This retrospective cohort study encompassed 7063 patients, among whom the in-hospital mortality stood at 12.2%. In the multivariate logistic regression, adjusted odds ratios (ORs) were contrasted with the reference category Q6 (8.8-9.1 mg/dL) for serum calcium levels and in-hospital mortality. The adjusted ORs for Q1 (≤ 7.7 mg/dL), Q2 (7.7-8 mg/dL), and Q7 (≥ 9.1 mg/dL) were 1.69 (95% CI 1.17-2.44, p = 0.005), 1.62 (95% CI 1.11-2.36, p = 0.013), and 1.57 (95% CI 1.1-2.24, p = 0.012) respectively. The dose-response analysis uncovered a U-shaped relationship between serum calcium levels and in-hospital mortality in diabetic patients with heart failure. Subgroup analyses confirmed result stability notwithstanding the influence of diverse factors. Our investigation revealed a U-shaped correlation between serum calcium levels and in-hospital mortality in diabetes patients with congestive heart failure, pinpointing a significant inflection point at 9.05 mg/dL.

Association between serum chloride and in-hospital mortality in congestive heart failure with diabetes: Data from the MIMIC-IV database.

Background: Congestive heart failure (CHF) demonstrates a heightened prevalence in individuals with diabetes mellitus within Intensive Care Units. The occurrence of abnormal chloride levels is frequently observed in critically ill patients, yet its clinical significance remains subject to debate. This study endeavors to explore the relationship between serum chloride levels and in-hospital mortality among patients affected by both congestive heart failure and diabetes. Methods: A retrospective cohort study was conducted, utilizing data from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database, focusing on adult patients in the United States. The impact of serum chloride levels upon ICU admission on in-hospital mortality was analyzed using multivariable logistic regression models, generalized additive models and subgroup analysis. Results: The study encompassed 7,063 patients with coexisting diabetes and congestive heart failure. The fully adjusted model revealed an inverse association between serum chloride levels and in-hospital mortality. As a tertile variable (Q3 vs Q1), the odds ratio (OR) was 0.73 with a 95% confidence interval (CI) of 0.54-0.98 (p = 0.039). As a continuous variable, per 1 mmol/L increment, the OR (95% CI) was 0.97 (0.96-0.99, p = 0.01). The relationship between serum chloride and in-hospital mortality demonstrated linearity (non-linear p = 0.958). Stratified analyses further validated the robustness of this correlation. Conclusions: Serum chloride levels exhibited a negative association with in-hospital mortality in patients with both congestive heart failure and diabetes. Nevertheless, prospective, randomized, controlled studies are warranted to corroborate and validate the findings presented in this investigation.

[Growth decline characteristics of Picea schrenkiana at different altitudes in Yili River Basin, western Tian-shan Mountains, Xinjiang, China]. / 新疆天山西部伊犁河流域不同海拔雪岭云杉生长衰退特征.

Picea schrenkiana is the dominant tree species in Ili River Basin located in the western Tianshan Mountains of Xinjiang. We investigated the growth decline characteristics of P. schrenkiana at different altitudes (1800, 2300 and 2800 m) based on tree-ring index (TRI) and percentage growth change (GC), aiming to understand the growth response of P. schrenkiana to drought events at different altitudes and the impacts of altitude on tree growth decline in this region. The results showed that P. schrenkiana experienced multiple decline events at low-altitude (1800 m). TRI and GC identified inconsistent occurrence time of the decline events. The variations of TRI indicated that P. schrenkiana at low-altitude experienced two large-scale declines during 1927-1933 and 2017-2014, respectively. The variations of GC identified four decline events, including 1891-1893, 1924-1926, 1973-1975, and 2004-2009. The radial growth of P. schrenkiana across altitudes from low to high was significantly affected by the Palmer drought severity index (PDSI) of the previous growing season. The impact of current PDSI on P. schrenkiana during the growing season initially enhanced but later decreased with increasing altitude. In the extreme drought year 1917, the magnitude of growth decline increased with altitude. At low-altitude (1800 m), the TRI was 0.65, which was 35% lower than the normal level. At mid-altitude (2300 m) and high-altitude (2800 m), it was 0.56 and 0.54, respectively, being 40% lower than the average level. The drought event in 1917 had a 2-year legacy effect on the growth of P. schrenkiana at all the altitudes, with the TRI in 1920 recovered to exceeding 0.9, being close to the normal level. The impact of altitude on drought-induced forest decline was significant. Tree growth in low-altitude areas was more vulnerable to drought events due to the relatively poorer water and temperature conditions at low-altitude, which could lead to multiple large-scale decline events. In mid- and high-altitude areas, where hydrothermal conditions were more favorable, trees could experience even more severe decline during extreme droughts.

Effects of percutaneous closure of atrial septal defects via the right internal jugular vein.

Background: Percutaneous atrial septal defect (ASD) closure is the preferred treatment for patients with suitable ASD anatomy. The safety and effectiveness of transcatheter closure have been established. However, reports on transesophageal echocardiography (TEE)-guided percutaneous closure of ASD via the right internal jugular vein (RIJV) are limited. The study aims to discuss the safety and effectiveness of percutaneous trans-jugular vein closure of ASD. Methods: We conducted a retrospective analysis of patients (n=103) with secondary ASD who underwent surgical treatment in the Department of Cardiovascular Surgery, the Second Hospital of Jilin University between July 2015 to July 2022. The article is a cross-sectional study. Clinical data, including age, gender, weight, defect diameter, tricuspid regurgitation, left atrial (LA) size, and the operation results, were collected and evaluated. Nonparametric rank sum tests were used to assess tricuspid regurgitation before and after surgery, while paired sample t-tests were used to compare LA size before and after surgery. Results: TEE-guided percutaneous closure of ASD via the RIJV was successfully performed in 97 out of 103 (94.2%) cases. The average procedure time was 34.48±13.06 min, and the mean age at the time of the procedure and ASD size were 36±18 years and 15.45±5.82 mm, respectively. On analyzing medical records and echocardiographic images, postoperative complications were found to occur in four (3.9%) patients. Among these, three patients had residual shunt as indicated by echocardiography during the operation, which subsequently disappeared at the three-month follow-up. One patient developed atrial fibrillation after surgery but returned to normal sinus rhythm with medication. Percutaneous closure of ASD via the RIJV was unsuccessful in 6 patients (5.8%), with 5 of them undergoing transthoracic ASD closure and achieving satisfactory results. One patient refused further surgical treatment. No pericardial effusion, thrombosis, atrioventricular block, or other complications were observed during the 3-month to 1-year follow-up period. Conclusions: ASD closure via the RIJV is a safe and effective therapeutic approach. The initial results are satisfactory, but further studies with large sample sizes and long-term follow-up are warranted to assess the long-term outcomes.

Research Progress on Aortic Root Aneurysms.

Aortic root aneurysms are one of the most common aortic root diseases, involving the aortic valve, aortic sinus, bilateral coronary arteries, and part of the ascending aorta. It is a life-threatening aortic disease with a high mortality rate of approximately 90%, due to aortic aneurysm rupture. Aortic valve insufficiency is one of the most common complications of aortic root aneurysms that can lead to acute left heart failure. The etiology of aortic root aneurysms is not yet completely clear and is mainly related to genetic diseases, such as Marfan syndrome and atherosclerosis. It can also occur secondary to aortic valve stenosis or a bivalve deformity. Surgery is the primary treatment for aortic root aneurysms, and aortic root replacement is a classic surgical method. However, the incidences of perioperative complications and mortality are relatively high, particularly in high-risk patients. In recent years, the anatomical structure of the aortic root has been gradually refined, and an in-depth understanding of root aneurysms has led to individualized treatment methods. Conservative drug therapy (ß-receptor blockers, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers), Bentall and modified Bentall surgeries (Button technology, Cabrol surgery, and modified Cabrol surgery), valve-sparing aortic root replacement (David and Yacoub), personalized external aortic root support, and endovascular intervention therapy have significantly improved the perioperative and long-term survival rates of patients with aortic root aneurysms. However, different treatment methods have their own advantages and disadvantages. This review aimed to summarize the current research progress and treatment of aortic root aneurysms.

Circular RNA MAP2K2-modified immunosuppressive dendritic cells for preventing alloimmune rejection in organ transplantation.

Long-term patient and graft survival has been achieved in organ transplantation but at the expense of toxic side effects that are associated with long-term use of nonspecific immunosuppressive drugs. Discovering new regulators of dendritic cells is the key for development of an ideal treatment to prevent immune rejection. We hypothesized that knockdown of circMAP2K2 induces immunosuppressive DCs and that treatment with circMAP2K2 silenced-DCs can prevent alloimmune rejection. DCs were cultured and transfected with siRNA for circMAP2K2. circMAP2K2 levels were measured by qRT-PCR. DC's maturation and immune function were assessed by flow cytometry and mixed lymphocyte reactions. The function of circMAP2K2 was illustrated by a series of RIP and IP. The therapeutics of engineered DCs was tested in a mouse heart transplantation model. We found that circMAP2K2 was highly expressed in mature DCs. Knockdown of circMAP2K2 reduced expression of MHCII, CD40 and CD80, attenuated the ability of DCs to activate allogeneic naïve T cells, and enhanced CD4+CD25+FOXP3+ regulatory T cells (Treg). circMAP2K2-induced immunosuppressive DCs by interacting with SENP3. Treatment with circMAP2K2-knockdown DCs attenuated alloimmune rejection and prolonged allograft survival in a murine heart transplantation model. The immune suppression induced in vivo was donor-antigen specific. In conclusion, knockdown of circMAP2K2 can induce immunosuppressive DCs which are able to inhibit overactive immune response, highlighting a new promising therapeutic approach for immune disorder diseases.

Association between dietary total choline and abdominal aorta calcification among older US adults: A cross-sectional study of the National Health and Nutrition Examination Survey.

BACKGROUND: Numerous studies indicate a potential bidirectional association between dietary choline intake and its derivative, betaine, and subclinical atherosclerosis. However, little research has been conducted on the relationship between dietary choline and severe abdominal aortic calcification (SAAC). METHODS: This cross-sectional study analyzed population-based data from the National Health and Nutrition Examination Survey (2013-2014). Choline intake and food sources were measured using two 24-h dietary-recall interviews. The abdominal aortic calcification score was measured using a dual-emission x-ray absorptiometry scan. To assess the relationship between choline intake and SAAC, the study utilized restricted cubic spline and a multivariable logistic regression model. RESULTS: Among the 2640 individuals included in the study, 10.9% had SAAC. After adjusting for all selected covariates, compared with the lowest quartile of dietary choline, the odds ratios of SAAC for the second-quartile, third-quartile, and fourth-quartile dietary choline intake were 0.63 (95% confidence interval [CI], 0.43-0.93), 0.63 (95% CI, 0.42-0.94), and 0.77 (95% CI, 0.5-1.16), respectively. The study found an L-shaped relationship between dietary choline and SAAC in the dose-response analysis. Subgroup analyses did not demonstrate any statistically significant interaction effects for any subgroup. CONCLUSION: The study found that a higher intake of dietary choline is associated with a lower prevalence of SAAC. The dose-response analysis revealed an L-shaped relationship between dietary choline and SAAC. However, further studies are warranted to investigate the direct role of choline in the development of SAAC.

Circ_0022920 Maintains the Contractile Phenotype of Human Aortic Vascular Smooth Muscle Cells Via Sponging microRNA-650 and Promoting Transforming Growth Factor Beta Receptor 1 Expression in Angiotensin II-Induced Models for Aortic Dissection.

Background Abnormal regulation of vascular smooth muscle cells is regarded as the iconic pathological change of aortic dissection (AD). Herein, we aim to identify circ_0022920 as a crucial regulator in AD. Methods and Results Microarray analysis of circular RNAs, messenger RNAs, and micro RNAs in patients with AD was performed, and we identified that circ_0022920 was significantly downregulated in these patients. The Pearson correlation analysis uncovered the negative correlation between miR-650 and circ_0022920 or TGFßR1 (transforming growth factor beta receptor 1). Angiotensin II was used to treat human aortic vascular smooth muscle cells (HASMCs) and mice as models for AD. Hematoxylin and eosin and Masson's trichrome staining were used to analyze AD histopathology. Cell proliferation was analyzed with Cell Counting Kit-8 assay and EdU incorporation. Cell migration was assessed with transwell and wound healing assays. Enhanced circ_0022920 expression dramatically inhibited HASMC proliferation and migration and maintained contractile marker expression induced by angiotensin II, whereas miR-650 exerted opposite effects. MiR-650 was a target of circ_0022920. MiR-650 targeted IRF1 (interferon regulatory factor 1) and thus negatively regulated TGFßR1 expression to promote HASMC proliferation and migration and inhibit contractile marker expression. Circ_0022920 suppressed the progression of AD in vivo. Conclusions Circ_0022920 modulates the contractile phenotype of HASMCs via regulating the miR-650-IRF1-TGFßR1 axis in angiotensin II-induced models for AD, which provides potential therapeutic targets for AD.

A comfort analysis of AR glasses on physical load during long-term wearing.

The present study investigated the effect of the physical load of augmented reality (AR) glasses on subjective assessments for an extended duration of a video viewing task. Ninety-six subjects were recruited for this test and were divided by spectacle use, sex, age, and body mass index (BMI). Four glasses frame weights were assessed. To investigate their effectiveness, a novel prototype adopting three design interventions, (1) adjustable frame width, (2) ergonomic temples, and (3) fixed centre of gravity, was designed with regard to subjective discomfort ratings (nose, ear, and overall). Subjective discomfort in all regions was significantly increased with increasing physical load on the nose. In addition, non-spectacle users, women, older users, and participants in the middle BMI category reported higher discomfort than other groups. This finding could have important implications for the ergonomic design of AR glasses and could help to identify design considerations relevant to the emerging wearable display industry. Practitioner summary: This research aims to explore the influence of the physical load of augmented reality (AR) glasses. It found that discomfort was increased with added nose load. Non-spectacle users, women, older users, and participants in the middle BMI category were more sensitive to discomfort. The results have important implications for glasses-type wearables' design.

In-ear earphone design-oriented pressure sensitivity evaluation on the external ear.

This study aimed to explore the pressure sensitivity of the external ear that can be the basis for adapting the pressure distribution on the concha for in-ear earphone design. Overall, 30 participants were included in this study, where an electronic mechanical algometer with a stepping motor was used to apply constant pressure. Before the experiment, the customised concha shell models of the participants were positioned in the ear perpendicular to the concha surface. Furthermore, the pressure discomfort threshold (PDT), moderate pressure discomfort (MPD), and maximum pressure threshold (MPT) in eight regions of the ear were recorded. This study's results indicate that the four regions of the external ear are less sensitive to pressure than those of the other regions. Additionally, women had higher pressure sensitivity values in the external ear. Therefore, this study's findings could have important implications for earphone designs and evaluating discomfort conditions in the external ear. Practitioner summary: This study explores the pressure sensitivity threshold (PDT, MPD, and MPT) on the external ear and the relevant implications for in-ear earphone design. Interestingly, regions closer to the bone structure were less sensitive to pressure, and men could tolerate greater pressure on the external ear than women.

ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis.

The endothelium is a single layer of epithelium covering the surface of the vascular system, and it represents a physical barrier between the blood and vessel wall that plays an important role in maintaining intravascular homeostasis. However, endothelial dysfunction or endothelial cell death can cause vascular barrier disruption, vasoconstriction and diastolic dysfunction, vascular smooth muscle cell proliferation and migration, inflammatory responses, and thrombosis, which are closely associated with the progression of several diseases, such as atherosclerosis, hypertension, coronary atherosclerotic heart disease, ischemic stroke, acute lung injury, acute kidney injury, diabetic retinopathy, and Alzheimer's disease. Oxidative stress caused by the overproduction of reactive oxygen species (ROS) is an important mechanism underlying endothelial cell death. Growing evidence suggests that ROS can trigger endothelial cell death in various ways, including pyroptosis, parthanatos, and ferroptosis. Therefore, this review will systematically illustrate the source of ROS in endothelial cells (ECs); reveal the molecular mechanism by which ROS trigger pyroptosis, parthanatos, and ferroptosis in ECs; and provide new ideas for the research and treatment of endothelial dysfunction-related diseases.

Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.

Cardiovascular diseases are the most common diseases threatening the health of the elderly, and the incidence and mortality rates associated with cardiovascular diseases remain high and are increasing gradually. Studies on the treatment and prevention of cardiovascular diseases are underway. Currently, several research groups are studying the role of exosomes and biomolecules incorporated by exosomes in the prevention, diagnosis, and treatment of clinical diseases, including cardiovascular diseases. Now, based on the results of published studies, this review discusses the characteristics, separation, extraction, and identification of exosomes, specifically the role of exosomal miRNAs in atherosclerosis, myocardial injury and infarction, heart failure, aortic dissection, myocardial fibrosis, ischemic reperfusion, atrial fibrillation, and other diseases. We believe that the observations noted in this article will aid in the prevention, diagnosis, and treatment of cardiovascular diseases.

Ministernotomy approach to aortic arch inclusion and frozen elephant trunk in the treatment of acute Stanford A aortic dissection.

This study aimed to report our results of ministernotomy approach to Liu's aortic root repair technique, Liu's aortic arch inclusion technique with frozen elephant trunk (FET) in the treatment in type A aortic dissection (TAAD). We retrospectively analyzed data on 68 Stanford A aortic dissection patients from October 2017 to March 2020. All patients underwent Liu's aortic root repair technique, Liu's aortic arch inclusion technique with FET and mild-moderate hypothermic circulatory arrest combined with ministernotomy approach. 154 TAAD patients between January 2014 and December 2016 underwent complete sternotomy were selected as control group. Clinical characteristics, data during operation, in-hospital and postoperative outcomes of these patients were observed. The mean hypothermic circulatory arrest time in ministernotomy Patients was 39.3 ± 7.9 min, aortic cross-clamp time was 105.9 ± 12.8 min, cardiopulmonary bypass time was 152.8 ± 24.3 min. Three patients died of multiple organ dysfunction syndrome in ministernotomy Patients. Perioperative temporary neurological dysfunction occurred in three (4.41%) patients, and 53 (77.9%) patients did not require any blood product transfusion during and after operation in ministernotomy Patients. Postoperative CT angiography (CTA) examination at 6-32 months showed excellent outcomes except in three (4.41%) cases where arch false lumen patency persisted. The Liu's aortic root repair technique, Liu's aortic arch inclusion technique with FET and mild-moderate hypothermia circulatory arrest simplify the surgical procedure and reduce bleeding, which can be accomplished through minimally invasive approach.

Hydrogen sulfide: A new therapeutic target in vascular diseases.

Hydrogen sulfide (H2S) is one of most important gas transmitters. H2S modulates many physiological and pathological processes such as inflammation, oxidative stress and cell apoptosis that play a critical role in vascular function. Recently, solid evidence show that H2S is closely associated to various vascular diseases. However, specific function of H2S remains unclear. Therefore, in this review we systemically summarized the role of H2S in vascular diseases, including hypertension, atherosclerosis, inflammation and angiogenesis. In addition, this review also outlined a novel therapeutic perspective comprising crosstalk between H2S and smooth muscle cell function. Therefore, this review may provide new insight inH2S application clinically.

Ex Vivo Hydrostatic Pressure Loading of Atrial Tissues Activates Profibrotic Transcription via TGF-ß Signal Pathway.

Excessive mechanical stress causes fibrosis-related atrial arrhythmia. Herein, we tried to investigate the mechanism of atrial fibrogenesis in response to mechanical stress by ex vivo approach. We collected atrial tissues from mice and then cultured them as "explants" under atmospheric pressure (AP group) or 50 mmHg hydrostatic pressure loading (HP group) conditions. Pathway-specific PCR array analysis on the expression of fibrosis-related genes indicated that the loading of atrial tissues to 50 mmHg for 24 hours extensively upregulated a series of profibrotic genes. qRT-PCR data also showed that loading atrial tissues to 50 mmHg enhanced Rhoa, Rock2, and Thbs1 expression at different time points. Interestingly, the enhanced expression of Thbs1 at 1 hour declined at 6-24 hours and then increased again at 72 hours. In contrast, an enhanced expression of Tgfb1 was observed at 72 hours. In contrast, daily loading to 50 mmHg for 3 hours significantly accelerated the outgrowth of mesenchymal stem-like stromal cells from atrial tissues; however, we did not observe significant phenotypic changes in these outgrowing cells. Our ex vivo experimental data clearly show the induction of profibrotic transcription of atrial tissues by HP loading, which confirms the common pathological feature of atrial fibrosis following pressure overload.

Drp1 regulates transcription of ribosomal protein genes in embryonic hearts.

Mitochondrial dysfunction causes severe congenital cardiac abnormalities and prenatal/neonatal lethality. The lack of sufficient knowledge regarding how mitochondrial abnormalities affect cardiogenesis poses a major barrier for the development of clinical applications that target mitochondrial deficiency-induced inborn cardiomyopathies. Mitochondrial morphology, which is regulated by fission and fusion, plays a key role in determining mitochondrial activity. Dnm1l encodes a dynamin-related GTPase, Drp1, which is required for mitochondrial fission. To investigate the role of Drp1 in cardiogenesis during the embryonic metabolic shift period, we specifically inactivated Dnm1l in second heart field-derived structures. Mutant cardiomyocytes in the right ventricle (RV) displayed severe defects in mitochondrial morphology, ultrastructure and activity. These defects caused increased cell death, decreased cell survival, disorganized cardiomyocytes and embryonic lethality. By characterizing this model, we reveal an AMPK-SIRT7-GABPB axis that relays the reduced cellular energy level to decrease transcription of ribosomal protein genes in cardiomyocytes. We therefore provide the first genetic evidence in mouse that Drp1 is essential for RV development. Our research provides further mechanistic insight into how mitochondrial dysfunction causes pathological molecular and cellular alterations during cardiogenesis.

Early outcomes with a hybrid technique for repair of a non-A non-B aortic dissection.

OBJECTIVE: This study reports the early outcomes of patients with acute non-A non-B aortic dissection that involved the aortic arch but not the ascending aorta. METHODS: From January 2013 to December 2018, 825 patients presented with aortic dissection. Of these, 28 patients with non-A non-B dissection (classified as dissection extending into the aortic arch with entry between the left common carotid artery and the left subclavian arteries) underwent a novel hybrid surgery. Self modified stent-grafts (Micropart Corp, Shanghai, China) were implanted via median sternotomy. Clinical presentation, postoperative data, and early outcomes were recorded. RESULTS: All patients underwent an emergency operation. There were no in-hospital mortalities, reexplorations for hemorrhage, reports of paraplegia, cerebral infarctions, endoleaks, or left subclavian artery occlusions. No blood products were required during or after the operations. During the early follow-up at 39.12 ± 15.04 months (6.0-74.0 months), 1 patient was lost to follow-up, and 1 patient died suddenly. Computed tomography angiography showed false lumen patency persisted in the aortic arch and descending aorta without any symptoms. The 6-month computed tomography angiography showed significantly smaller distal aortic arch diameters (31.94 ± 6.95 mm) and descending aorta diameters (34.84 ± 4.15 mm) than measured preoperatively (36.76 ± 4.15 mm and 37.31 ± 4.7 mm, respectively). No paraplegia, cerebral infarction, upper limb ischemia, or left subclavian artery ischemia events were reported. CONCLUSIONS: Our inclusion aortic arch technique is a safe, effective, and simple treatment for non-A non-B aortic dissections that can avoid endoleaks, requires no blood products, and has satisfactory early outcomes.

Preventing alloimmune rejection using circular RNA FSCN1-silenced dendritic cells in heart transplantation.

BACKGROUND: While heart transplantation is used as a standard treatment for heart failure, transplant rejection continues to pose a challenge. Recent evidence has shown that circular RNA (circRNA) is a new type of gene regulator in cell development. Our aim was to demonstrate that treatment with tolerogenic dendritic cells (Tol-DCs) generated by circular RNA FSCN1 (circFSCN1) silencing could prevent alloimmune rejection and prolong heart graft survival in heart transplantation. METHODS: Bone marrow-derived DCs were transfected with circFSCN1 siRNA in vitro. The circFSCN1 level was measured by qRT-PCR. DC maturation was determined by flow cytometry. Mixed lymphocyte reactions (MLRs) were conducted to assess the function of DCs to activate T cells and to generate regulatory T cells (Tregs). In situ RNA hybridization and fluorescent microscopy were performed to detect the distribution of circFSCN1 in DCs. A heterotopic allogeneic murine heart transplantation was conducted where recipients were pre-treated with donor derived circFSCN1-silenced Tol-DCs. Heartbeat was monitored to assess immune rejection. RESULTS: Exonic circFSCN1 was highly expressed in the cytoplasm of mature DCs. Knockdown of circFSCN1 using siRNA arrested DCs at an immature state, impaired DC's ability to activate T cells and enhanced Treg generation. Treatment with circFSCN1-silenced Tol-DCs prevented alloimmune rejection, prolonged allograft survival, reduced fibrosis, and induced Tregs in vivo. CONCLUSIONS: Knockdown of circFSCN1 induces Tol-DCs and treatment with these Tol-DCs prevents alloimmune rejection and prolongs allograft survival. This is a promising therapeutic target to combat transplant rejection in heart transplantation and increases our understanding of circRNA in the immune system.

Novel hybrid treatment for extensive aortic arch aneurysms, a case report.

BACKGROUND: The treatment for extensive aortic arch aneurysms involving the aortic arch and descending aorta is challenging for most cardiovascular surgeons. The surgical treatment is associated with a very high mortality rate. The optimal treatment has not been defined. CASE PRESENTATION: A 49-year-old male was hospitalized due to chest and upper back pain. Computed tomography angiography (CTA) demonstrated there was an extensive aortic arch aneurysm extending to the left common carotid artery and descending aorta. A novel single- stage hybrid surgery was performed on the patient through two steps: treatment of the aortic arch through median sternotomy and thoracic endovascular artery repair. The patient recovered uneventfully. CONCLUSIONS: Our single-stage hybrid repair approach is safe, simple and effective. It provides an alternative treatment for extensive aortic arch aneurysms.

LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.

Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. We integrated the mRNA microarray data set with GSE52093 to determine the differentially expressed genes. Bioinformatic analysis, including Gene Expression Omnibus 2R, Venn diagram analysis, gene ontology, pathway enrichment, and protein-protein interaction networks were used to identify the target lncRNA, microRNA, and mRNA involved in AD. Subsequently, we validated the bioinformatics data using techniques in molecular biology in human tissues and VSMCs. Linc01278, microRNA-500b-5p, and ACTG2 played an important role in the vascular smooth muscle contraction pathway. Linc01278 and ACTG2 were downregulated and miR-500b-5p was upregulated in AD tissues. Molecular markers of VSMC phenotypic switching, including SM22α, SMA, calponin, and MYH11, were downregulated in AD tissues. Plasmid-based overexpression and RNA interference-mediated downregulation of linc01278 weakened and enhanced VSMC proliferation and phenotypic switching, respectively. Dual-luciferase reporter assays confirmed that linc01278 regulated miR-500b-5p that directly targeted ACTG2 in HEK293T cells. Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD.