Emergent surgical retrieval of a left atrial appendage occluder migrated into the left ventricular outflow tract with secondary massive mitral regurgitation: A case report and literature review.

Thrombotic complications of atrial fibrillation continue to pose a significant challenge in clinical practice today. Left atrial appendage occlusion (LAAO) has emerged as a promising alternative to oral anticoagulation for high-risk patients with atrial fibrillation. However, despite the potential benefits, there is still the possibility of life-threatening complications such as device dislocation. In this case study, we present a patient who experienced severe hemodynamic disturbances due to the embolization of LAAO device into the left ventricular outflow tract, resulting in a torn mitral valve and secondary massive mitral regurgitation, just 3 hours after the procedure. As a result, emergent surgical intervention was required to remove the device and repair the mitral valve. We also conducted a review of previous studies on the retrieval of dislodged left atrial appendage occluders through surgical procedures. It is crucial to maintain vigilance, foster interdisciplinary collaboration, and respond promptly to ensure the safety and efficacy of LAAO procedures.

MiR-22-3p in exosomes increases the risk of heart failure after down-regulation of FURIN.

Heart failure (HF) is often the inevitable manifestation of myocardial ischemia. Hypoxia can induce cardiomyocytes to express many microRNAs (miRNAs), which are highly expressed in exosomes. In addition, miR-22-3p is a marker in heart failure. Therefore, miR-22-3p was taken as the research object to explore its role and mechanism in HF. HF differentially expressed miRNAs were screened by bioinformatic analysis. The HF rats model was constructed and identified by detecting serum brain natriuretic peptide (BNP) and ultrasound analysis [left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS)]. The extracted exosomes were identified by transmission electron microscopy, and Western blot was used to detect the expressions of Tsg101 and CD63. Quantitative real-time polymerase chain reaction detected miR-22-3p expression in serum, exosomes, and serum without exosomes, while the cardiomyocytes cytotoxicity was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and PKH26 staining. After overexpressing/silencing miR-22-3p in cells, cell viability, apoptosis, and apoptosis-associated markers were detected. Bioinformatic analysis screened the target gene of miR-22-3p, which was verified by dual-luciferase assay. Regulation of miR-22-3p on FURIN was measured by rescue tests. In vivo experiments were verified the above results. MiR-22-3p was identified as the research object. BNP was increased in the model group, while LVEF and LVFS were decreased. MiR-22-3p was overexpressed in HF-treated serum and exosomes. Normal exosomes did not affect cardiomyocyte function, while high concentrations of HF-treated exosomes were cytotoxic. By regulating apoptosis-related genes, overexpressed miR-22-3p inhibited cell activity and promoted cell apoptosis. Silenced miR-22-3p with opposite effects counteracted effects of HF-treated exosomes. FURIN, target gene of miR-22-3p, was negatively regulated by miR-22-3p, while overexpressed FURIN promoted cell activity and inhibited apoptosis. In vivo research was consistent with the results of cell experiments. By regulating FURIN, miR-22-3p in exosomes increases the risk of HF damage.

Homing of the bone marrow-derived interstitial cells of Cajal is decreased in diabetic mouse intestine.

BACKGROUND: Interstitial cells of Cajal (ICCs), which express c-Kit receptor tyrosine kinase (KIT), play an important role in gastrointestinal motility. Loss of ICCs likely contributes to diabetic gastrointestinal motility disorder, however, the mechanism of attrition remains unknown. Here, we test the hypothesis that the bone marrow-derived progenitors are an important source of intestinal ICCs and that decreased homing of these progenitors in diabetes contributes to ICC diminution. METHODS: Wild type mice were X-ray irradiated, transplanted with bone marrow (BMT) from green fluorescence protein (GFP)-transgenic (TG)-mice and subsequently made diabetic by streptozotocin (STZ) injection. Intestinal homing of GFP-positive bone marrow-derived cells was examined 2 or 5 months after STZ treatment. RESULTS: In the BMT-mice, we found many GFP-positive bone marrow-derived cells (BMDCs) in most parts of the intestinal area, the number of BMDCs was significantly decreased in diabetic mice compared with nondiabetic controls. As a representative area, we further examined the myenteric plexus of the proximal small intestine, and found that the cell numbers of ICCs marked by c-Kit-positive immunoreactivity were decreased by more than 40% in diabetic versus nondiabetic mice. Furthermore, numbers of c-Kit+/GFP+ and c-Kit+/GFP- cells were similar in nondiabetic mice, and decreased by 45.8% and 42.0%, respectively, in diabetic mice. CONCLUSION: These results suggest that the decreased homing from the bone marrow is a major cause of ICC loss in the intestine in diabetes mellitus.

Activation of dissolved molecular oxygen by Cu(0) for bisphenol a degradation: Role of Cu(0) and formation of reactive oxygen species.

In this study, Cu(0) was synthesized with NaBH4 as a reducing agent for Cu(II) and used to activate dissolved molecular oxygen (O2) under acidic conditions. The Cu(0) synthesized had much higher activity than the purchased. The roles of Cu was clarified and the formation of reactive oxygen species was discussed through direct detection for the first time. By detecting the valence change of Cu in a CuO system, Bisphenol A (BPA) was found to accelerate the transformation of Cu(II) to Cu(I). Besides, the evidence from electron spin resonance (ESR) studies and scavenging tests revealed the new roles of Cu(0) that Cu(0) could not only convert O2 to produce ·O2-, but also catalyze H2O2 to ·OH. The results from this study offer evidence of new reaction pathways in Cu-activated O2 systems and deepen understanding of the reaction between Cu species and O2.

[Effect of ginsenoside Rh2 on transplanted-tumor and expression of JAM in mice].

OBJECTIVE: To discuss the anti-tumor activity of ginsenoside Rh2, we observed the expressions of the junction adhesion molecul (JAM) in transplanted-tumor in mice. METHOD: The models of 40 transplanted-tumor mice that were established by subsequently injecting cancer ascite of mice (S180) with 0.2 mL per mouse into the preepipodite skin were divided into two groups. Experiment group was drenched with 2 mL ginsenoside Rh2 per mouse, equating to a dose 20 mg x kg(-1). Control group was drenched with 2 mL normal saline per mouse. The expression of JAM-1, JAM-2 in the lymphatics, blood vessels and tumours were observed by immunohistochemical staining. RESULT: The expression of JAM-1 on the cancer cells was significantly decreased in experiment group (IA 340.55) as compared with control group (IA 549.90, P<0.05). However, JAM-2 weakly expressed in both two groups. The density of blood vessels in which JAM-1, JAM-2 expressed showed 2.33 and 1.34 in control group, and 1.09 and 0.9 in experiment group respectively. Moreove, the density of lymph vessels were respectively 2.23 and 1.88 in control group compared with 0.99 and 0.79 in experiment group. The expression in blood vessels and lymph vessels in control group were significantly higher than those in experiment group, respectively (P<0.05). CONCLUSION: Ginsenoside Rh2 can affect the tumor growth, further angiogenesis and lymphangiogenesis by down-regulating JAM expression in tumor.

Mental health literacy among residents in Jiaxing City / 预防医学

Objective@# To investigate the level of mental health literacy among residents in Jiaxing City, Zhejiang Province, so as to provide insights into implementation of mental health education and improvements of the quality of mental health services. @*Methods@#A total of 2 248 permanent residents at ages of 18 years and older were sampled using a multi-stage stratified random sampling method from 3 streets (townships) in Jiaxing City. Residents' demographics were collected using self-designed questionnaires, and the mental health literacy was investigated using the Mental Health Literacy Questionnaire. Factors affecting the achievement of the target of mental health literacy were identified among residents using a multivariable logistic regression model. @*Results@#A total of 2 248 questionnaires were allocated and 2 172 valid questionnaires were recovered, with an effective recovery rate of 96.62%. The respondents included 1 075 men (49.49%) and 1 097 women (50.51%). There were 623 respondents that met the target of the mental health literacy (28.68%). Multivariable logistic regression analysis showed a higher possibility of achieving the target of mental health literacy levels among women than among men (OR=1.282, 95%CI: 1.047-1.570), among unmarried residents (OR=1.685, 95%CI: 1.018-2.788) than among married residents, among residents with educational levels of junior high school (OR=1.689, 95%CI: 1.168-2.441), high school/vocational high school/technical secondary school (OR=2.420, 95%CI: 1.601-3.658) and college or above (OR=3.543, 95%CI: 2.252-5.574) than among residents with an educational level of primary and below, among students (OR=2.572, 95%CI: 1.013-6.527), medical personnel (OR=3.330, 95%CI: 2.029-5.467), teachers (OR=2.909, 95%CI: 1.202-7.040), freelance/self-employed staff (OR=1.519, 95%CI: 1.100-2.098) and other professional technical personnel (OR=1.529, 95%CI: 1.012-2.310) than among workers.@* Conclusions @#The proportion of mental health literacy levels meeting the target is high among residents in Jiaxing City, and gender, educational level, occupation and marital status are factors affecting mental health literacy levels.

Enhanced degradation of chloramphenicol at alkaline conditions by S(-II) assisted heterogeneous Fenton-like reactions using pyrite.

The Fenton-like reactions catalyzed by pyrite can efficiently degrade organic contaminants by oxidation process. When chloramphenicol (CAP) was exposed to the pyrite-H2O2 system, the CAP removal rate rapidly reached 100% however slowed to a halt at alkaline conditions. Results indicated that by adding S(-II) in pyrite-H2O2 system improved the oxidation efficiency of CAP at alkaline conditions. The transformation of S22- and Sn2- observed by X-ray photoelectron spectroscopy (XPS), confirmed that amorphous iron polysulfide (FeSn) was freshly generated on the pyrite surface. The availability of S(-II) promoted the generation of FeSn. Besides, S(-II) played a role in accelerating the Fe(III)/Fe(II) cycles. The potential of S(-II) activating H2O2 to generate hydroxyl radicals (OH), which was confirmed by electron spin resonance (ESR) spectroscopy, quenching experiments, and trapping experiments, have supported the proposed mechanisms. This study came up with an efficient way of enhancing Fenton-like reactions by pyrite catalyzed at alkaline conditions, by adding S(-II) in the system. The new findings have implications for sulfide minerals, their interactions with pollutants, and the transformation products of sulfur in systems where Fe species are also present.

Sequestration of chelated copper by structural Fe(II): Reductive decomplexation and transformation of Cu(II)-EDTA.

Chelated coppers, such as Cu(II)-EDTA, are characteristically refractory and difficult to break down because of their high stability and solubility. Cu(II)-EDTA sequestration by structural Fe(II) (Fe(II)) was investigated intensively in this study. Up to 101.21mgCu(II)/gFe(II) was obtained by Fe(II) in chelated copper sequestration under near neutral pH condition (pH 7.70). The mechanism of Cu(II)-EDTA sequestration by Fe(II) was concluded as follows: 3Cu(II)-EDTA+7Fe(II)+9H2O → Cu(0)↓+ Cu2O↓(the major product)+2Fe2O3·H2O↓+3Fe(II)-EDTA +14H(+) Novel results strongly indicate that Cu(II) reductive transformation induced by surface Fe(II) was mainly responsible for chelated copper sequestration. Cu(0) generation was initially facilitated, and subsequent reduction of Cu(II) into Cu(I) was closely combined with the gradual increase of ORP (Oxidation-Reduction Potential). Cu-containing products were inherently stable, but Cu2O would be reoxidized to Cu(II) with extra-aeration, resulting in the release of copper, which was beneficial to Cu reclamation. Concentration diminution of Cu(II)-EDTA within the electric double layer and competitive adsorption were responsible for the negative effects of Ca(2+), Mg(2+). By generating vivianite, PO4(3-) was found to decrease surface Fe(II) content. This study is among the first ones to identify the indispensible role of reductive decomplexation in chelated copper sequestration. Given the high feasibility and reactivity, Fe(II) may provide a potential alternative in chelated metals pollution controlling.

[Comparative analysis on meteorological condition for persistent haze cases in summer and winter in Beijing].

Summer is another peak season for haze besides winter in Beijing area, which is different from that in South China. The data of microwave radiometer, profiler, sounding, AWS, NCEP (NCAR) and air pollution monitors were used in the analysis of two haze cases which occurred in winter and summer, respectively. Both cases lasted for 6 days. This research focused on the difference in the mechanism of the formation and persistence of haze cases in various seasons. In winter, north-westerly flow dominated Beijing at upper-levels and a few of shallow troughs passed by during persistent haze development. The main meteorological reasons for lower visibility in 6 days were: there was an inversion in the boundary layer all the time; wind was weak at surface and moisture went up gradually. The change of inversion height and humidity day and night led to the diurnal variation of PM2.5 concentration and visibility. The surface wind speed kept lower because the weak cold air could not often hit the surface during the haze case. In addition, three factors played key roles in the inversion formation in boundary layer. One was that the rapid decrease in the surface temperature after sunset due to the radiation. At the same time, there was some warm advection at upper boundary layer. The third one attributed to the temperature increase after the air flowing over the mountains and down. However, in summer, regional transportation of aerosol, sustained convective stability and high air saturation were very important factors for the haze formation. Under the sub-tropic high control, the wind direction at lower troposphere was south. The PM2.5 concentration went up when the speed of south wind increased. The south flow caused by both synoptic scale systems and mountain-valley breeze near Beijing transported the aerosol northward from higher polluted area. There was no inversion in the summer haze case. But, the convective inhibition was kept over 200 J x kG(-1). As the result, it was not favorable for the pollutant diffusion upward. Furthermore, the level of free convection also changed during the day and at the night, which had similar effect on the PM2.5 concentration and visibility as the daily variation of inversion. In conclusion, these cases in winter and summer were categorized into two different kinds of persistent haze. The main reason leading to the difference was the synoptic pattern.

COX-2-mediated regulation of VEGF-C in association with lymphangiogenesis and lymph node metastasis in lung cancer.

The mechanisms underlying the effects of COX-2 on tumor lymphangiogenesis remain largely undefined. Here, the human lung cancer cell lines A549, 95D, Anip973, and AGZY83-a with different metastatic capacities were investigated by immunostaining, western blotting, and real-time RT-PCR. We observed increased expressions of COX-2 and VEGF-C in the three highly metastatic cell lines compared with the less metastatic AGZY83-a cell line. The COX-2-specific inhibitor Celecoxib suppressed VEGF-C expression whereas the main COX-2 metabolite PGE(2) elevated VEGF-C expression in Anip973 and AGZY83-a cells in positive and negative experiments. To determine the functional link to COX-2 more specifically and elucidate the mechanistic pathway, we used a siRNA to knock down the high COX-2 expression in Anip973 cells and transfected a COX-2 cDNA to enhance the low COX-2 expression in AGZY83-a cells, and then treated the cells with EP1/EP4 agonists or antagonists, respectively. The results revealed that the EP1/EP4 agonists significantly increased VEGF-C production in the COX-2-knockdown Anip973 cells. In contrast, the EP1/EP4 antagonists diminished VEGF-C production in the COX-2-overexpressing AGZY83-a cells. Furthermore, animal models provided evidence that Celecoxib decreased VEGF-C expression, lymphangiogenesis, and lymph node metastases in Anip973 cells, whereas PGE(2) treatment increased the same factors in the parental AGZY83-a cells. A positive correlation between COX-2 and VEGF-C was also confirmed in vivo. The present data suggest that COX-2 regulates VEGF-C expression via the PGE(2) pathway, and that EP1/EP4 receptors are involved in PGE(2)-mediated VEGF-C production. Thus, COX-2 may represent a candidate gene for blocking tumor lymphangiogenesis and lymph node metastasis.

Ultrastructure changes of cardiac lymphatics during cardiac fibrosis in hypertensive rats.

Hypertension is one of the most common diseases that induce a series of pathological changes in different organs of the human body, especially in the heart. There is a wealth of evidence about blood vessels in hypertensive myocardium, but little is known about structural changes in the cardiac lymphatic system. To clarify the changes in structure of the cardiac lymphatic system during hypertension, we developed a hypertension animal model with Dahl S rats and we used Dahl R rats as the control group. We examined the expression of collagen fibers, atrial natriuretic peptide, connexin43, and LYVE-1 in the rat heart by immunohistochemistry. The ultrastructure of the cardiac lymphatics was detected by transmission electron microscopy and scanning electron microscopy. We demonstrated extensive lymphatic fibrosis in the hearts of the Dahl S hypertension group, characterized by increased thin collagen fibrils that connected with the lymphatics directly. Ultrastructural changes in the cardiac lymphatic endothelium such as an increase of vesicles and occurrence of vacuoles, active exocytosis, and cytoplasmic processes, restored the draining of tissue fluid. Our study suggests that during hypertension, the changes in structure of the cardiac lymphatics may be one important factor involved in cardiac fibrosis. Therefore, the lymphatics may be a possible target for reducing fibrosis in the treatment of hypertension.

Inhibition of cyclooxygenase-2 suppresses lymph node metastasis via VEGF-C.

Most experimental work addressing cyclooxygenase-2 (COX-2) inhibitor has focused on suppressing hematogenic spread. Little is known about the mechanism by which this inhibitor can also block lymphatic metastasis. Here, the effects of COX-2 inhibitor on vascular endothelial growth factor-C (VEGF-C) expression, lymphangiogenesis and lymph node metastasis were investigated. Utilizing the highly metastatic human lung adenocarcinoma cell line Anip973 and its parental line AGZY83-a, which has a low metastatic capacity, we found elevated VEGF-C and COX-2 immunoreactivity in Anip973 cells compared with AGZY83-a cells. Celecoxib down-regulated expression of VEGF-C mRNA and protein in Anip973 cells while PGE(2) up-regulated expression of VEGF-C mRNA and protein in AGZY83-a cells in a concentration-dependent manner. The expression of COX-2 and VEGF-C was significantly increased in xenografted Anip973 tumors compared with AGZY83-a tumors. The Anip973 tumors showed more lymphatic vessels and lymph node metastasis than the AGZY83-a tumors. In vivo, celecoxib decreased VEGF-C expression in Anip973 tumor-treated mice to a similar level to that in the AGZY83-a tumor-treated mice. Consistent with this decrease in VEGF-C expression, the density of lymphatic vessels and lymph node metastasis in Anip973 tumor-treated mice were suppressed to approximately that found in the AGZY83-a tumor-treated ones. Taken together, our results suggest that the differential expression of COX-2 and VEGF-C might help explain the different metastasis phenotype of lung adenocarcinoma cancer, and that COX-2 inhibitor mediates VEGF-C to block lymphangiogenesis and lymph node metastasis. Thus, COX-2 may be a potential therapeutic target for blocking lymph node metastasis in lung adenocarcinoma.

Independently tunable 1.3 W femtosecond Ti:sapphire lasers passively synchronized with attosecond timing jitter and ultrahigh robustness.

A stable passively synchronized femtosecond laser has been realized by coupling two 1.3 W mode-locked Ti:sapphire lasers with a Kerr medium. An ultralong tolerance of 10 microm for the cavity length mismatch and a timing jitter of less than 0.4 fs were obtained. The relative carrier-envelope phase slip was directly observed by measuring the heterodyne output between the two lasers.

Morphologic features of lymphatic in periphery region of gastric carcinoma and colon carcinoma.

BACKGROUND & OBJECTIVE: Most of the studies on lymphatic metastasis mechanism of carcinoma are confined to distribution of lymphatics. This research was to observe distribution and morphologic features of the lymphatics in periphery region of carcinoma, and morphologic changes of lymphatic endothelia. METHODS: Specimens were obtained from 10 patients with gastric carcinoma and 10 patients with colon carcinoma; 20 mice models bearing colon carcinoma were established. Morphology of lymphatics and ultrastructure of lymphatic endothelia were observed under microscope. Number density and volume density of lymphatics in periphery region of carcinoma and normal region were measured using computer image analysis system; open rate and destructive rate of lymphatics were calculated. RESULTS: The lymphatics in periphery region of carcinoma were dilated; their walls were disintegrated. Lymphatic endothelia were dissolved and destroyed into broken fragments; the organellae showed pathologic changes. Number density and volume density of lymphatics were significantly higher in periphery region of colon carcinoma than in normal region [(10.2+/-1.7)/mm(2) vs. (5.1+/-0.8)/mm(2), P < 0.05û (1.5+/-0.2)% vs. (0.7+/-0.0)%, P < 0.05], and were significantly higher in periphery region of gastric carcinoma than in normal region [(8.0+/-0.9)/mm(2) vs. (3.4+/-0.6)/mm(2), P < 0.01; (1.6+/-0.3)% vs. (0.8+/-0.2)%, P < 0.05]. Open rate of lymphatics was significantly higher in periphery regions of mice model colon carcinoma, human gastric carcinoma, and colon carcinoma than in relevant normal regions (22.2% vs. 7.8%, 35.0% vs. 8.0%, and 25.8% vs. 5.0%, P < 0.05). Destructive rate of lymphatics was significantly higher in periphery regions of mice model colon carcinoma, and human gastric carcinoma than in relevant normal regions (20.1% vs. 0, and 35.3% vs. 2.0%, P < 0.05). CONCLUSION: Compare with the lymphatics in normal tissue, the lymphatics in periphery region of carcinoma tissue are dilated with disintegrated walls; the lymphatic endothelia are destroyed; the density of the lymphatics is increased.