Infliximab modifies CD74-mediated lymphatic abnormalities and adipose tissue alterations in creeping fat of Crohn's disease.

BACKGROUND: Lymphatic abnormalities are essential for pathophysiologic changes of creeping fat (CrF) in Crohn's disease (CD). Anti-tumor necrosis factor (TNF) therapy has been proved to alleviate CrF lesions, however, whether it achieves these by remodeling lymphatics is unknown. METHODS: CD74 expression was detected in CrF and uninvolved mesentery of CD patients. Lymphatic functions in vitro were evaluated and lymphatic endothelium barrier were checked by transendothelial electrical resistance (TEER) and FITC-Dextran permeability. Protein level of tight junction and signaling pathways were detected by western blotting. RESULTS: CD74 was upregulated in LECs of CrF and positively correlated with TNF-α synthesis. This was suppressed by IFX administration. In vitro, TNF-α stimulated LECs to express CD74 through NF-κB signaling pathway, and this was rescued by IFX. CD74 downregulation suppressed the abilities of LECs in proliferation, migration and tube formation. Interaction of CD74-MIF impaired LECs' barrier via reducing tight junction proteins in an ERK1/2-dependent manner, which was reversed by CD74 downregulation. Consistently, the CD patients receiving IFX therapy displayed decreased lymphangiogenesis and improved mesenteric lymphatic endothelium barrier, companied with reduced adipocyte size and adipokine levels in CrF. CONCLUSIONS: Anti-TNF therapy could modify pathological changes in CrF by alleviating CD74-mediated lymphatic abnormalities.

Urban airborne PM2.5 induces pulmonary fibrosis through triggering glycolysis and subsequent modification of histone lactylation in macrophages.

Airborne fine particulate matter (PM2.5) can cause pulmonary inflammation and even fibrosis, however, the underlying molecular mechanisms of the pathogenesis of PM2.5 exposure have not been fully appreciated. In the present study, we explored the dynamics of glycolysis and modification of histone lactylation in macrophages induced by PM2.5-exposure in both in vivo and in vitro models. Male C57BL/6 J mice were anesthetized and administrated with PM2.5 by intratracheal instillation once every other day for 4 weeks. Mouse RAW264.7 macrophages and alveolar epithelial MLE-12 cells were treated with PM2.5 for 24 h. We found that PM2.5 significantly increased lactate dehydrogenase (LDH) activities and lactate contents, and up-regulated the mRNA expression of key glycolytic enzymes in the lungs and bronchoalveolar lavage fluids of mice. Moreover, PM2.5 increased the levels of histone lactylation in both PM2.5-exposed lungs and RAW264.7 cells. The pro-fibrotic cytokines secreted from PM2.5-treated RAW264.7 cells triggered epithelial-mesenchymal transition (EMT) in MLE-12 cells through activating transforming growth factor-ß (TGF-ß)/Smad2/3 and VEGFA/ERK pathways. In contrast, LDHA inhibitor (GNE-140) pretreatment effectively alleviated PM2.5-induced pulmonary inflammation and fibrosis via inhibiting glycolysis and subsequent modification of histone lactylation in mice. Thus, our findings suggest that PM2.5-induced glycolysis and subsequent modification of histone lactylation play critical role in the PM2.5-associated pulmonary fibrosis.

Paeonol inhibits melanoma growth by targeting PD1 through upregulation of miR-139-5p.

The abnormal immune response mediated by malignant melanoma is related to PD1. Paeonol has pharmacological antitumor activity. Previous studies have indicated that paeonol induces tumor cell apoptosis, but its underlying mechanism in tumor immunity remains unknown. In this study, malignant melanoma was established in normal and thymectomized mice to determine the important role of the thymus in the antitumor effects of paeonol. Paeonol-treated thymocytes were cocultured with melanoma cell spheres to further evaluate the regulatory role of thymocytes in tumor immune dysfunction. Studies have shown that PD1 may be targeted by miR-139-5p. Our results revealed that tumor-induced thymic atrophy was significantly accompanied by high PD1 expression and low miR-139-5p expression. Interestingly, paeonol significantly reversed thymic atrophy and largely protected thymocytes against low PD1 expression and high miR-139-5p expression. Dual-luciferase assays indicated that miR-139-5p interacted with the 3' untranslated region (3'-UTR) of PD1. These results showed that paeonol alleviates PD1-mediated antitumor immunity by reducing miR-139-5p expression and demonstrated a novel mechanism for melanoma immunotherapy.

Metagenomic analysis reveals taxonomic and functional diversity of microbial communities on the deteriorated wall paintings of Qinling Tomb in the Southern Tang Dynasty, China.

The microbial colonization on ancient murals attracts more and more attention since the threaten by microorganisms was first reported in Lascaux, Spain. However, the biodeterioration or biodegradation of mural paintings resulted by microorganisms is not clear yet. Especially the biological function of microbial communities in different conditions remained largely unaddressed. The two mausoleums of the Southern Tang Dynasty are the largest group of emperor mausoleums during the Five Dynasties and Ten Kingdoms period in China, which are of great significance to the study of the architecture, imperial mausoleum systems and art in the Tang and Song Dynasties. To make clear the species composition and metabolic functions of different microbial communities (MID and BK), we analyzed the samples from the wall paintings in one of the two mausoleums of the Southern Tang Dynasty with metagenomics method. The result showed totally 55 phyla and 1729 genera were detected in the mural paintings. The two microbial community structure were similar with the dominance of Proteobacteria, Actinobacteria and Cyanobacteria. However, the species abundance presented a significant difference between two communities at genus level --- MID is Lysobacter, Luteimonas are predominant in MID while Sphingomonas and Streptomyces are popular in BK, which is partially attributed to the different substrate materials of murals. As a result, the two communities presented the different metabolic patterns that MID community was mainly participated in the formation of biofilm as well as the degradation of exogenous pollutants while the BK was predominantly related to the photosynthesis process and biosynthesis of secondary metabolites. Taken together, these findings indicated the effect of environmental factor on the taxonomic composition and functional diversity of the microbial populations. The installation of artificial lighting needs to be considered carefully in the future protection of cultural relics.

Observation of Electronic Strong Correlation in VTe_{2}-2sqrt[3]×2sqrt[3] Monolayer.

Strong electron correlation under two-dimensional limit is intensely studied in the transition metal dichalcogenides monolayers, mostly within their charge density wave (CDW) states that host a star of David period. Here, by using scanning tunneling microscopy and spectroscopy and density functional theory calculations with on-site Hubbard corrections, we study the VTe_{2} monolayer with a different 2sqrt[3]×2sqrt[3] CDW period. We find that the dimerization of neighboring Te-Te and V-V atoms occurs during the CDW transition, and that the strong correlation effect opens a Mott-like full gap at Fermi energy (E_{F}). We further demonstrate that such a Mott phenomenon is ascribed to the combination of the CDW transition and on-site Coulomb interactions. Our work provides a new platform for exploring Mott physics in 2D materials.

Intraoperative crystalloid-colloid infusion ratio associated with the development of early surgical complications after ileal pouch-anal anastomosis in ulcerative colitis: a multicenter long-term follow-up study.

BACKGROUND: Intraoperative intravenous fluid administration proves to be associated with surgical patients' postoperative outcomes. Few studies reported the relationship between intraoperative crystalloid-colloid infusion ratio and early surgical complications after ileal pouch-anal anastomosis (IPAA) in ulcerative colitis (UC). METHODS: Data on patients with underwent IPAA from January 2008 to March 2022 at our three inflammatory bowel disease (IBD) surgery centers were retrospectively collected. Intraoperative anesthetic data were recorded and later evaluated by our team anesthesiologist. RESULTS: A total of 140 eligible patients with a median follow-up time of 6.0 years [interquartile range (IQR): 2.0-8.0] were enrolled. Among all enrolled patients, 34 (24.3%) developed early surgical complications after IPAA. Greater blood loss and lower crystalloid-colloid infusion ratio were observed in patients with early surgical complications. Crystalloid-colloid infusion ratio < 2 and blood loss ≥ 200 ml had the most significant area under the receiver-operating characteristic curve (AUC) of 0.664 and 0.674 in predicting early surgical complications. Crystalloid-colloid infusion ratio < 2 [odds ratio (OR), 2.571; 95% confidence intervals (CI), 1.067-6.195, p = 0.035] and blood loss ≥ 200 ml (OR, 3.165; 95% CI, 1.288-7.777, p = 0.012) were independent risk factors for the development of early post-IPAA complications. CONCLUSION: Intraoperative crystalloid-colloid infusion ratio < 2 and blood loss volume over 200 ml during IPAA contribute to the occurrence of early surgical complications. Early attentions and necessary interventions are warranted to avoid these risk factors during the IPAA surgery in order to prevent the development of early surgical complications.

Calycosin protects against oxidative stress-induced cardiomyocyte apoptosis by activating aldehyde dehydrogenase 2.

Myocardial infarction (MI) is the leading cause of death worldwide, and oxidative stress is part of the process that causes MI. Calycosin, a naturally occurring substance with cardioprotective properties, is one of the major active constituents in Radix Astragali. In this study, effect of Calycosin was investigated in vivo and in vitro to determine whether it could alleviate oxidative stress and oxidative stress-induced cardiac apoptosis in neonatal cardiomyocytes (NCMs) via activation of aldehyde dehydrogenase 2 (ALDH2). Calycosin protected against oxidative stress and oxidative stress-induced apoptosis in NCMs. Molecular docking revealed that the ALDH2-Calycosin complex had a binding energy of -9.885 kcal/mol. In addition, molecular docking simulations demonstrated that the ALDH2-Calycosin complex was stable. Using BLI assays, we confirmed that Calycosin could interact with ALDH2 (KD  = 1.9 × 10-4 M). Furthermore, an ALDH2 kinase activity test revealed that Calycosin increased ALDH2 activity, exhibiting an EC50 of 91.79 µM. Pre-incubation with ALDH2 inhibitor (CVT-10216 or disulfiram) reduced the cardio-protective properties Calycosin. In mice with MI, Calycosin therapy substantially reduced myocardial apoptosis, oxidative stress, and activated ALDH2. Collectively, our findings clearly suggest that Calycosin reduces oxidative stress and oxidative stress-induced apoptosis via the regulation of ALDH2 signaling, which supports potential therapeutic use in MI.

Microparticles from Hyperphosphatemia-Stimulated Endothelial Cells Promote Vascular Calcification Through Astrocyte-Elevated Gene-1.

Endothelial microparticles (EMPs) can be released in chronic kidney disease (CKD). Plasma concentration of high inorganic phosphate (HP) is considered as a decisive determinant of vascular calcification in CKD. We therefore explored the role of HP-induced EMPs (HP-EMPs) in the vascular calcification and its potential mechanism. We observed the shape of HP-EMPs captured by vascular smooth muscle cells (VSMCs) dynamically changed from rare dots, rosettes, to semicircle or circle. Our results demonstrated that HP-EMPs could directly promote VSMC calcification, or accelerate HP-induced calcification through signal transducers and activators of transcription 3 (STAT3)/bone morphogenetic protein-2 (BMP2) signaling pathway. AEG-1 activity was increased through HP-EMPs-induced VSMC calcification, in arteries from uremic rats, or from uremic rats treated with HP-EMPs. AEG-1 deficiency blocked, whereas AEG-1 overexpression exacerbated, the calcium deposition of VSMCs. AEG-1, a target of miR-153-3p, could be suppressed by agomiR-153-3p. Notably, VSMC-specific enhance of miR-153-3p by tail vein injection of aptamer-agomiR-153-3p decreased calcium deposition in both uremia rats treated with HP-EMPs or not. HP-EMPs could directly induce VSMCs calcification and accelerate Pi-induced calcification, and AEG-1 may act as crucial regulator of HP-EMPs-induced vascular calcification. This study sheds light on the therapeutic agents that influence HP-EMPs production or AEG-1 activity, which may be of benefit to treat vascular calcification.

Dimethylarginine dimethylaminohydrolase 1 protects PM2.5 exposure-induced lung injury in mice by repressing inflammation and oxidative stress.

BACKGROUND: Airborne fine particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5) pollution is associated with the prevalence of respiratory diseases, including asthma, bronchitis and chronic obstructive pulmonary disease. In patients with those diseases, circulating asymmetric dimethylarginine (ADMA) levels are increased, which contributes to airway nitric oxide deficiency, oxidative stress and inflammation. Overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1), an enzyme degrading ADMA, exerts protective effects in animal models. However, the impact of DDAH1/ADMA on PM2.5-induced lung injury has not been investigated. METHODS: Ddah1-/- and DDAH1-transgenic mice, as well as their respective wild-type (WT) littermates, were exposed to either filtered air or airborne PM2.5 (mean daily concentration ~ 50 µg/m3) for 6 months through a whole-body exposure system. Mice were also acutely exposed to 10 mg/kg PM2.5 and/or exogenous ADMA (2 mg/kg) via intratracheal instillation every other day for 2 weeks. Inflammatory response, oxidative stress and related gene expressions in the lungs were examined. In addition, RAW264.7 cells were exposed to PM2.5 and/or ADMA and the changes in intracellular oxidative stress and inflammatory response were determined. RESULTS: Ddah1-/- mice developed more severe lung injury than WT mice after long-term PM2.5 exposure, which was associated with greater induction of pulmonary oxidative stress and inflammation. In the lungs of PM2.5-exposed mice, Ddah1 deficiency increased protein expression of p-p65, iNOS and Bax, and decreased protein expression of Bcl-2, SOD1 and peroxiredoxin 4. Conversely, DDAH1 overexpression significantly alleviated lung injury, attenuated pulmonary oxidative stress and inflammation, and exerted opposite effects on those proteins in PM2.5-exposed mice. In addition, exogenous ADMA administration could mimic the effect of Ddah1 deficiency on PM2.5-induced lung injury, oxidative stress and inflammation. In PM2.5-exposed macrophages, ADMA aggravated the inflammatory response and oxidative stress in an iNOS-dependent manner. CONCLUSION: Our data revealed that DDAH1 has a marked protective effect on long-term PM2.5 exposure-induced lung injury.

Changes in the live birth profile in Henan, China: A hospital registry-based study.

BACKGROUND: Preterm complications and neonatal asphyxia are the leading causes of death in those under 5 years of age. However, little information exists for the province of Henan, China. The purpose of this study was to explore changes in the live birth profile in a provincial hospital over the past 32 years in Henan, China. METHODS: A retrospective analysis was conducted to reveal the characteristics of live neonates from 1987 to 2018. RESULTS: There were 118 253 live births during the period, including 19 798 (16.74%) preterm births. The neonatal death rate was 6.45‰, and the top risk factor was preterm birth complications and birth asphyxia. Before 1998, neonatal death occurred primarily among term infants. Between 1999 and 2018, preterm infants, especially extreme and very preterm infants with very low birthweight, constituted more than half of all mortalities, and the preterm birth rate increased from 5.94% in 1999 to 16.69% in 2018. The risk factors associated with preterm birth were being male (aOR = 1.18, P < 0.001), advanced maternal age (>35 years old; aOR = 1.08, P = 0.008), gravidity ≥2 (aOR = 1.15, P < 0.001), parity ≥2 (aOR = 1.50, P < 0.001), placenta previa (aOR = 7.41, P < 0.001), twin or multiple births (aOR = 10.63, P < 0.001), hypertension (aOR = 2.08, P < 0.001), and rupture of membrane (aOR = 5.03, P < 0.001). CONCLUSIONS: The preterm birth rate has increased over the past 32 years from 4.98% to 16.69% in a provincial hospital in China. Preterm birth was the leading reason for neonatal death, and birth asphyxia was the major risk factor for death in term infants.

Coexistence of Superconductivity and Nontrivial Band Topology in Monolayered Cobalt Pnictides on SrTiO3.

As an intrinsically layered material, FeSe has been extensively explored for potentially revealing the underlying mechanisms of high transition temperature (high-Tc) superconductivity and realizing topological superconductivity and Majorana zero modes. Here we use first-principles approaches to identify that the cobalt pnictides of CoX (X = As, Sb, Bi), none of which is a layered material in bulk form. Nevertheless, all can be stabilized as monolayered systems either in freestanding form or supported on the SrTiO3(001) substrate. We further show that each of the cobalt pnictides may potentially harbor high-Tc superconductivity beyond the Cu- and Fe-based superconducting families, and the underlying mechanism is inherently tied to their isovalency nature with the FeSe monolayer. Most strikingly, each of the monolayered CoX's on SrTiO3 is shown to be topologically nontrivial, and our findings provide promising new platforms for realizing topological superconductors in the two-dimensional limit.

Chinese universities' special programs supporting talents to seek a United Nations career: a center-periphery-model analysis.

In recent years, China's higher education sector has started to establish special programs to train and support talents to seek career opportunities in the United Nations (UN). To explore these special programs and understand their relationship with China's internationalization strategies and its higher education, we used the center-periphery model as the theoretical framework. We analyzed 53 institutional documents and conducted semi-structured interviews among 5 university staff members and 21 students/recent graduates who were involved in these special programs. The analysis on the special programs implied Chinese higher education's peripheral position in supporting talents to work in the UN. This was reflected by the conforming practice, including accepting current UN recruitment regulations and English's dominance in the UN recruitment practice. However, we also identified alternative dynamics that China and its higher education do not simply obey the center-periphery model and accept their peripheral status. Instead, special programs were established to achieve China's global strategy of moving to the center of international arena via multilateralism and international organizations such as the UN. This study sheds light on further explorations of the state-university relationship in China in the globalization era, especially from the perspective of cultural diplomacy and soft power.

Dauricine inhibits proliferation and promotes death of melanoma cells via inhibition of Src/STAT3 signaling.

Melanoma is the most common type of skin cancer. Signal transducer and activator of transcription 3 (STAT3) signaling has been demonstrated to be a therapeutic target for melanoma. Dauricine (Dau), an alkaloid compound isolated from the root of Menispermum dauricum DC., has shown tumor-suppressing effects in multiple human cancers, but its potential in melanoma remains unexplored. In this study, we demonstrated that Dau significantly inhibited the viability and proliferation of A375 and A2058 melanoma cells. Death of melanoma cells was also markedly promoted by Dau. Moreover, Dau inhibited phosphorylation-mediated activation of STAT3 and Src in a dose-dependent manner. Notably, constitutive activation of Src partially abolished the antiproliferative and cytotoxic activities of Dau on melanoma cells. Molecular docking showed that Dau could dock on the kinase domain of Src with a binding energy of -10.42 kcal/mol. Molecular dynamics simulations showed that Src-Dau binding was stable. Surface plasmon resonance imaging analysis also showed that Dau has a strong binding affinity to Src. In addition, Dau suppressed the growth of melanoma cells and downregulated the activation of Src/STAT3 in a xenograft model in vivo. These data demonstrated that Dau inhibits proliferation and promotes cell death in melanoma cells by inhibiting the Src/STAT3 pathways.

Surgical Septal Myectomy for the Treatment of Residual Left Ventricular Outflow Tract Obstruction Following Failed Alcohol Septal Ablation.

The reasons of residual left ventricular outflow tract (LVOT) obstruction following alcohol septal ablation (ASA) remain unclear, and outcomes of myectomy following failed ASA remain underreported.Thirteen symptomatic patients (10 women, a median age of 60.0 years) who underwent septal myectomy following failed ASA were reviewed. The patients were followed up for a median of 6 months. The clinical characteristics and outcomes of these patients were analyzed and were compared with those of 178 patients who underwent isolated myectomy without previous ASA at our institution during the same period.In the first ASA procedure, the median number of septal perforator arteries injected was 1.0 with the median value of peak creatine kinase following ablation of 978.5 U/L.Uncontrollable extent and location of infarcted myocardium caused by ablation and mitral subvalvular anomalies were found in four (30.8%) and seven (53.8%) patients, respectively. No operative or follow-up deaths occurred. The median maximum LVOT gradients fell from preoperative 112.0 to 8.5 mmHg at follow-up (P < 0.001). Compared with controls, patients with failed ASA had a higher proportion of mitral subvalvular anomalies (53.8% versus 13.5%, P = 0.001) and developed a higher incidence of complete atrioventricular block following myectomy (15.4% versus 1.7%, P = 0.038).Low institutional or operator experience with ablation, uncontrollable extent and location of infarcted myocardium caused by ablation, and mitral subvalvular anomalies may be reasons for failed ASA. Surgical myectomy for the treatment of residual LVOT obstruction after unsuccessful ASA may be associated with favorable results.

Ovarian Dysfunction Induced by Chronic Whole-Body PM2.5 Exposure.

Fine particulate matter (PM2.5) pollution arouses public health concerns over the world. Increasing epidemiologic evidence suggests that exposure to ambient airborne PM2.5 increases the risk of female infertility. However, relatively few studies have systematically explored the harmful effect of chronic PM2.5 exposure on ovarian function and the underlying mechanisms. In this study, female C57BL/6J mice are exposed to filtered air or urban airborne PM2.5 for 4 months through a whole-body exposure system. It is found that PM2.5 exposure significantly caused the alteration of estrus cycles, reproductivity, hormone levels, and ovarian reserve. The granulosa cell apoptosis via the mitochondria dependent pathway contributes to the follicle atresia. With RNA-sequencing technique, the differentially expressed genes induced by PM2.5 exposure are mainly enriched in ovarian steroidogenesis, reactive oxygen species and oxidative phosphorylation pathways. Furthermore, it is found that increased PM2.5 profoundly exacerbated ovarian oxidative stress and inflammation in mice through the NF-κB/IL-6 signaling pathway. Notably, dietary polydatin (PD) supplement has protective effect in mice against PM2.5-induced ovarian dysfunction.These striking findings demonstrate that PM2.5 and/or air pollution is a critical factor for ovarian dysfunction through mitochondria-dependent and NF-κB/IL-6-mediated pathway, and PD may serve as a pharmaceutic candidate for air pollution-associated ovarian dysfunction.

Exploring High Transition Temperature Superconductivity in a Freestanding or SrTiO_{3}-Supported CoSb Monolayer.

As a two-dimensional entity, FeSe has been widely explored to harbor high transition temperature (high-T_{c}) superconductivity in diverse physical settings; yet to date, the underlying superconducting mechanisms are still under active debate. Here we use first-principles approaches to identify a chemically different yet structurally identical counterpart of FeSe, namely, monolayered CoSb, which is shown to be an attractive candidate to harbor high-T_{c} superconductivity as well. We first show that a freestanding CoSb monolayer can adopt the FeSe-like layered structure, even though its known bulk phase has no resemblance to layering. Next, we demonstrate that such a CoSb monolayer possesses superconducting properties comparable with or superior to FeSe, a striking finding that can be attributed to the isovalency nature of the two systems. More importantly, the layered CoSb structure can be stabilized on SrTiO_{3}(001), offering appealing alternative platforms for realizing high-T_{c} superconductivity beyond the well-established Cu- and Fe-based superconducting families. CoSb/SrTiO_{3}(001) also exhibits distinctly different magnetic properties from FeSe/SrTiO_{3}(001), which should provide a crucial new angle to elucidate the microscopic mechanisms of superconductivity in these and related systems.

The Role of Cariporide in Protecting Saphenous Vein among Different Aldehyde Dehydrogenase Genotypes.

OBJECTIVE: We aimed to study the effect of cariporide (CP) on protecting the saphenous vein and the role of acetaldehyde dehydrogenase 2 (ALDH2) in coronary artery bypass grafting (CABG). BACKGROUND: The saphenous vein is the main graft material used in CABG. Recent studies suggested that CP is effective in protecting against various cardiovascular diseases. METHODS: Segments of a surgically removed saphenous vein were used to examine the vascular response to CP. The ALDH2 genotype and expression of related proteins were assessed by Western blotting and immunohistochemistry. RESULTS: Among the conditions tested, the University of Wisconsin solution with CP (4°C, 5 min) treatment showed the best protective effect on the saphenous vein. The incidence of major adverse cardiac events was higher in the ALDH2-GA (heterozygous mutant) genotype population after CABG. CONCLUSION: CP plays a role in reducing the production of reactive oxygen species and apoptosis by ALDH2-mediated mitochondrial function improvement. The ALDH2 mutant genotype might be one of the risk factors for coronary atherosclerotic heart disease.

Predictors of ischemic mitral regurgitation improvement after surgical revascularization plus mitral valve repair for moderate ischemic mitral regurgitation.

BACKGROUND AND AIM: Ischemic mitral regurgitation (IMR) recurrence after combined coronary artery bypass grafting (CABG) and mitral valve repair does occur, with a prevalence of 20% to 30% at the 2- to 4-year follow-up. This single-center study aims to identify the predictors of IMR improvement after surgical revascularization plus mitral valve repair for moderate IMR. METHODS: A total of 201 eligible patients were entered into an improved group (n = 141) or a control group (n = 60) according to whether moderate or more mitral regurgitation occurred at the 2-year postoperative time point. Clinical outcomes between groups were compared. RESULTS: The left ventricular endo-diastolic diameter (LVEDD), type of ring (rigid complete ring), and the use of repair techniques (restrictive annuloplasty associated with subvalvular and/or leaflet repair) were three predictors of IMR improvement after surgery (odds ratio [OR] = 0.921, 95% confidence interval [CI], 0.865-0.976, P = .025; OR = 7.753, 95% CI, 3.168-17.742, P < .001; and OR = 0.168, 95% CI, 0.076-0.423, P = .004, respectively). The cutoff value of the LVEDD was 65 mm with a sensitivity of 80.0% and a specificity of 65.2%. Patients in the improved group compared with those in the control group demonstrated better cumulative survival during a median follow-up of 41.0 months (χ2 = 4.559, logrank P = .033) and a reduced ratio of the New York Heart Association class III-IV at the latest follow-up (5.7% vs 38.4%, P < .001). CONCLUSIONS: An LVEDD of less than 65 mm, the use of a rigid complete ring, and combined restrictive annuloplasty and subvalvular and/or leaflet repair are associated with IMR improvement after CABG plus mitral valve repair for the treatment of moderate IMR; IMR improvement 2 years after surgery is associated with improved midterm outcomes.

Surgical treatment of symptomatic left anterior descending myocardial bridges: myotomy vs. bypass surgery.

PURPOSE: To compare the effects of myotomy and bypass surgery for treating myocardial bridges (MBs) over the left anterior descending artery (LAD) in a single-center observation study. METHODS: Fifty-four eligible patients (34 males, median age of 60 years old) with symptomatic LAD-MBs who underwent myotomy (31 patients) or bypass surgery (23 patients) were included in this study. The primary endpoints were the occurrence of major adverse cardiac events (MACEs) and angiographic demonstration of adverse angiographic results. RESULTS: No surgical death was observed. During a median follow-up of 26 months, 11 patients developed MACEs (7.4% for myotomy vs. 40.9% for bypass surgery, p = 0.007). Surgical strategy (bypass surgery vs. myotomy) was an independent risk factor for MACEs (odds ratio = 3.681, 95% confidence interval 1.814-8.685, p = 0.011). Myotomy compared with bypass surgery had a significantly lower incidence of adverse angiographic results (3.7% of residual compression vs. 40.9% of LIMA graft failure, p = 0.003). Among ten patients suffering from LAD-MBs with concomitant proximal coronary stenosis who underwent bypass surgery, only one reported transient recurrent exertional chest pain, and all LIMA grafts were patent. CONCLUSIONS: Myotomy of symptomatic LAD-MBs may be associated with encouraging midterm results. Bypass surgery may be recommended for treating symptomatic LAD-MBs with concomitant proximal coronary stenosis.

Impacts of Skeletonized Bilateral Internal Mammary Artery Bypass Grafting on the Risk of Deep Sternal Wound Infection.

This single-center study aimed to evaluate the incidence of deep sternal wound infection (DSWI) following skeletonized bilateral internal mammary artery (BIMA) harvest in a Chinese cohort. Using propensity score matching, this study also provided a present-day assessment of the impacts of skeletonized BIMA grafting versus skeletonized single internal mammary artery (SIMA) grafting on early outcomes.From January 2014 to December 2017, 2403 eligible patients were entered into either a BIMA group (n = 368) or a SIMA group (n = 2035). The incidence of DSWI was recorded. Analysis of early outcomes was further performed for propensity score-matched (1:1) cohorts.The BIMA group received a similar incidence of DSWI as did the SIMA group (1.6% versus 0.9%, P = 0.247). No significant differences between subgroup diabetic-BIMA, subgroup nondiabetic-BIMA, subgroup diabetic-SIMA, and subgroup nondiabetic-SIMA were found regarding the incidence of DSWI (2.0%, 1.4%, 1.0%, and 0.7%, respectively; P > 0.05 between groups). After matching, treatment type (skeletonized BIMA grafting versus skeletonized SIMA grafting) was not an independent risk factor for postoperative DSWI (OR = 1.309, 95% CI 0.897-2.714, P = 0.704) or predictors of other early outcomes. Additionally, the two matched groups shared similar early outcomes (including postoperative DSWI), regardless of whether or not the merger with diabetes (all P > 0.05).Skeletonized BIMA harvest as compared with skeletonized SIMA harvest was not associated with an increased risk of DSWI, regardless of whether or not the merger with diabetes. Patients with skeletonized BIMA grafting received similar surgical mortality and major postoperative morbidity as did matched patients with skeletonized SIMA grafting.