Polar-coded channel polarization for reducing complexity of soft-decision forward error correction.

To reduce the computational complexity of soft-decision (SD) forward error correction (FEC), we propose a polar coding method with a low-complexity successive cancellation decoder. Polar coding induces channel polarization in which two bit-channels with lower and higher reliabilities are polarized. Only the less-reliable bit-channels are protected by SD-FEC, whereas the more-reliable bit-channels are offloaded, reducing the complexity of SD-FEC decoding. The degradation of the bit error ratio (BER) performance can be suppressed by designing the polar encoder structures for the successive cancellation decoder. We numerically demonstrate that the proposed method manages to both reduce the computational complexity by half and suppress the BER performance degradation by less than 0.6 dB, compared with the conventional method using only the SD-FEC.

Deciphering the Morphological Difference of Amyloid-ß Fibrils in Familial and Sporadic Alzheimer's Diseases.

The aggregation of amyloid-ß (Aß) into amyloid fibrils is the major pathological hallmark of Alzheimer's disease (AD). Aß fibrils can adopt a variety of morphologies, the relative populations of which are recently found to be associated with different AD subtypes such as familial and sporadic AD (fAD and sAD, respectively). The two AD subtypes differ in their ages of onset, AD-related genetic predispositions, and dominant Aß fibril morphologies. We postulate that these disease subtype-dependent fibril morphology differences can be attributed to the intrinsic fibril properties and interacting molecules in the environment. Using atomistic discrete molecular dynamics simulations, we demonstrated that the fAD-dominant morphology exhibited a lower free-energy barrier for fibril growth but also a lower stability compared with the sAD-dominant fibril morphology, resulting in the time-dependent population change consistent with experimental observations. Additionally, we studied the effect of the Bri2 BRICHOS domain, an endogenous protein that has been reported to inhibit Aß aggregation by preferential binding to fibrils, as one of the possible environmental factors. The Bri2 BRICHOS domain showed stronger binding to the fAD-dominant fibril than the sAD-dominant fibril in silico, suggesting a more effective suppression of fAD-dominant fibril formation. This result explains the high population of the sAD-dominant fibril morphology in sporadic cases with normal Bri2 functions. Genetic predisposition in fAD, on the other hand, might impair or overwhelm Bri2 functions, leading to a high population of fAD-associated fibril morphology. Together, our computational findings provide a theoretical framework for elucidating the AD subtypes entailed by distinct dominant amyloid fibril morphologies.

Safety and effectiveness of left atrial appendage closure in atrial fibrillation patients with different types of heart failure.

BACKGROUND: Both atrial fibrillation (AF) and heart failure (HF) are common cardiovascular diseases. If the two exist together, the risk of stroke, hospitalization for HF and all-cause death is increased. Currently, research on left atrial appendage closure (LAAC) in patients with AF and HF is limited and controversial. This study was designed to investigate the safety and effectiveness of LAAC in AF patients with different types of HF. METHODS: Patients with non-valvular atrial fibrillation (NVAF) and HF who underwent LAAC in the First Affiliated Hospital of Army Medical University from August 2014 to July 2021 were enrolled. According to left ventricular ejection fraction (LVEF), the study divided into HF with reduced ejection fraction (LVEF < 50%, HFrEF) group and HF with preserved ejection fraction (LVEF ≥ 50%, HFpEF) group. The data we collected from patients included: gender, age, comorbid diseases, CHA2DS2-VASc score, HAS-BLED score, NT-proBNP level, residual shunt, cardiac catheterization results, occluder size, postoperative medication regimen, transthoracic echocardiography (TTE) results and transesophageal echocardiography (TEE) results, etc. Patients were followed up for stroke, bleeding, device related thrombus (DRT), pericardial tamponade, hospitalization for HF, and all-cause death within 2 years after surgery. Statistical methods were used to compare the differences in clinical outcome of LAAC in AF patients with different types of HF. RESULTS: Overall, 288 NVAF patients with HF were enrolled in this study, including 142 males and 146 females. There were 74 patients in the HFrEF group and 214 patients in the HFpEF group. All patients successfully underwent LAAC. The CHA2DS2-VASc score and HAS-BLED score of HFrEF group were lower than those of HFpEF group. A total of 288 LAAC devices were implanted. The average diameter of the occluders was 27.2 ± 3.5 mm in the HFrEF group and 26.8 ± 3.3 mm in the HFpEF group, and there was no statistical difference between the two groups (P = 0.470). Also, there was no statistically significant difference in the occurrence of residual shunts between the two groups as detected by TEE after surgery (P = 0.341). LVEF was significantly higher in HFrEF group at 3 days, 3 months and 1 year after operation than before (P < 0.001). At 45-60 days after surgery, we found DRT in 9 patients and there were 4 patients (5.4%) in HFrEF group and 5 patients (2.3%) in HFpEF group, with no significant difference between the two groups (P = 0.357). One patient with DRT had stroke. The incidence of stroke was 11.1% in patients with DRT and 0.7% in patients without DRT (P = 0.670). There was one case of postoperative pericardial tamponade, which was improved by pericardiocentesis at 24 h after surgery in the HFpEF group, and there was no significant difference between the two groups (P = 1.000). During a mean follow-up period of 49.7 ± 22.4 months, there were no significant differences in the incidence of stroke, bleeding, DRT and HF exacerbation between the two groups. We found a statistical difference in the improvement of HF between HFrEF group and HFpEF group (P < 0.05). CONCLUSIONS: LAAC is safe and effective in AF patients with different types of HF. The improvement of cardiac function after LAAC is more pronounced in HFrEF group than in HFpEF group.

Deficiency of neuropeptide Y attenuates neointima formation after vascular injury in mice.

BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) limits therapeutic revascularization. Neuropeptide Y (NPY), co-stored and co-released with the sympathetic nervous system, is involved in this process, but its exact role and underlying mechanisms remain to be fully understood. This study aimed to investigate the role of NPY in neointima formation after vascular injury. METHODS: Using the left carotid arteries of wild-type (WT, NPY-intact) and NPY-deficient (NPY-/-) mice, ferric chloride-mediated carotid artery injury induced neointima formation. Three weeks after injury, the left injured carotid artery and contralateral uninjured carotid artery were collected for histological analysis and immunohistochemical staining. RT-qPCR was used to detect the mRNA expression of several key inflammatory markers and cell adhesion molecules in vascular samples. Raw264.7 cells were treated with NPY, lipopolysaccharide (LPS), and lipopolysaccharide-free, respectively, and RT-qPCR was used to detect the expression of these inflammatory mediators. RESULTS: Compared with WT mice, NPY-/- mice had significantly reduced neointimal formation three weeks after injury. Mechanistically, immunohistochemical analysis showed there were fewer macrophages and more vascular smooth muscle cells in the neointima of NPY-/- mice. Moreover, the mRNA expression of key inflammatory markers such as interleukin-6 (IL-6), transforming growth factor-ß1 (TGF-ß1), and intercellular adhesion molecule-1 (ICAM-1) was significantly lower in the injured carotid arteries of NPY-/- mice, compared to that in the injured carotid arteries of WT mice. In RAW264.7 macrophages, NPY significantly promoted TGF-ß1 mRNA expression under unactivated but not LPS-stimulated condition. CONCLUSIONS: Deletion of NPY attenuated neointima formation after artery injury, at least partly, through reducing the local inflammatory response, suggesting that NPY pathway may provide new insights into the mechanism of restenosis.

Continuous Hypobaric Hypoxia may Promote Atherosclerosis Progression in Apolipoprotein E-deficient Mice.

Background: Intermittent normobaric hypoxia can promote the progression of atherosclerotic plaques. However, the effect of continuous hypobaric hypoxia (CHH), which is a major feature of high-altitude environment, on atherosclerosis has not been investigated thoroughly. Materials and Methods: After eight weeks of high-cholesterol diet, 30 male ApoE-/- mice were randomly divided into control and CHH groups. Mice in the CHH group lived in a hypobaric chamber with an oxygen content of 10% and air pressure of 364 mmhg (equal to 5,800 m altitude above sea level) for 4 weeks, while mice in the control group lived in normoxia condition. Then all mice were euthanized and the atherosclerotic lesion size and plaque stability in the aortic root were assessed. Intraplaque angiogenesis was characterized by immunostaining of CD31 and endomucin, which are identified as specific markers of vascular endothelial cells. Immunohistochemistry and qRT-PCR were performed to measure inflammatory cytokines. Results: Four weeks of CHH exposure promoted the growth of atherosclerotic lesions (p=0.0017) and decreased the stability of atherosclerotic plaques. In CHH group, plaque smooth muscle cells and collagen contents decreased, while plaque macrophages and lipids contents increased significantly (p<0.001). The contents of CD31 (p=0.0379) and endomucin (p=0.0196) in the plaque was higher in the CHH group and correlated with angiogenesis progression. Further, the content of monocyte chemotactic protein-1 (p=0.0376) and matrix metalloproteinase-2 was significantly higher (p=0.0212) in the CHH group. Conclusions: CHH may accelerate atherosclerosis progression in ApoE-/- mice by promoting angiogenesis and inflammation.

Arcuate NPY is involved in salt-induced hypertension via modulation of paraventricular vasopressin and brain-derived neurotrophic factor.

Chronic high salt intake is one of the leading causes of hypertension. Salt activates the release of the key neurotransmitters in the hypothalamus such as vasopressin to increase blood pressure, and neuropepetide Y (NPY) has been implicated in the modulation of vasopressin levels. NPY in the hypothalamic arcuate nucleus (Arc) is best known for its control in appetite and energy homeostasis, but it is unclear whether it is also involved in the development of salt-induced hypertension. Here, we demonstrate that wild-type mice given 2% NaCl salt water for 8 weeks developed hypertension which was associated with marked downregulation of NPY expression in the hypothalamic Arc as demonstrated in NPY-GFP reporter mice as well as by in situ hybridization analysis. Furthermore, salt intake activates neurons in the hypothalamic paraventricular nucleus (PVN) where mRNA expression of brain-derived neurotrophic factor (BDNF) and vasopressin was found to be upregulated, leading to elevated serum vasopressin levels. This finding suggests an inverse correlation between the Arc NPY level and expression of vasopressin and BDNF in the PVN. Specific restoration of NPY by injecting AAV-Cre recombinase into the Arc only of the NPY-targeted mutant mice carrying a loxP-flanked STOP cassette reversed effects of salt intake on vasopressin and BDNF expression, leading to a normalization of salt-dependent blood pressure. In summary, our study uncovers an important Arc NPY-originated neuronal circuitry that could sense and respond to peripheral electrolyte signals and thereby regulate hypertension via vasopressin and BDNF in the PVN.

High-frequency fiber Bragg gating accelerometer and strain sensor-based blast test on a concrete slab.

The blast test is the most direct method of measuring explosive performance and structural safety. Because of long-distance wires and electromagnetic interference, some scattering exists in the blast test using electrical sensors. For this paper, a double-hinge high-frequency fiber Bragg gating (FBG) accelerometer was designed and manufactured to measure the acceleration on a blast-loaded concrete slab. The resonance frequency and sensitiveness of the sensor were determined as 3400 Hz and 6.26 pm/g, respectively. Blasting was performed seven times, with each blast generating the energy equivalent of 50 kg of TNT. The stress waves were obtained from the blast source for distances at 4 m, 6 m, and 8 m. The peak accelerations in test 6 were obtained as 396.21 g, 123.57 g, and 38.88 g, respectively, whereas the propagation velocity of the stress wave was around 2500 m/s. Furthermore, the study was complemented by numerical simulations. The test results were compared with the empirical formula, which validated the reliability and applicability of fiber optical sensors in blast testing. The proposed fiber optical sensors have shown promising results, further boosting their practical applications in blast testing and monitoring structural health following a blast shock.

NPY promotes macrophage migration by upregulating matrix metalloproteinase-8 expression.

Macrophage migration is thought to participate in obesity-related cardiovascular diseases. Matrix metalloproteinase-8 (MMP-8) possesses proteolytic activity on the extracellular matrix (ECM), which promotes macrophage migration to the site of vascular injury. Neuropeptide Y (NPY) is a bioactive peptide involved in MMP expression. However, it is uncertain whether NPY can regulate the expression of matrix metalloproteinase-8 (MMP-8) in macrophages. In this study, wild-type C57BL/6 and NPY-/- mice were fed a high-fat diet and subjected to subcutaneous carotid artery injury with ferric chloride, to observe the role of NPY and macrophages in neointima formation. In addition, Raw264.7 cells were treated with NPY and its antagonists to observe MMP-8 expression and macrophage migration. We found that NPY-/- mice exhibited significantly reduced neointima formation after carotid artery injury. The content of macrophages and MMP-8 in the neointima and media were also significantly reduced in NPY-/- mice compared with C57BL/6 mice. Moreover, the expression of MMP-8 in macrophages was also decreased in NPY-/- mice. NPY increased MMP-8 messenger RNA and protein expression in Raw264.7 cells in vitro, and this effect was abrogated by the Y1R antagonist. In addition, NPY increased the phosphorylation of ERK1/2, which was significantly attenuated by co-treatment with the Y1R antagonist. Moreover, NPY-induced MMP-8 expression could be decreased by the ERK1/2 inhibitor PD98059. Furthermore, NPY promoted macrophage migration across type I collagen in vitro. In conclusion, NPY promotes macrophage migration by upregulating MMP-8 expression, which we believe to be an underappreciated mechanism of the increased progression of neointima formation.

Characteristics and long-term survival of patients with chronic thromboembolic pulmonary hypertension in China.

BACKGROUND AND OBJECTIVE: The purpose of this study was to report the characteristics and long-term survival of patients with CTEPH treated in three distinct ways: PEA, BPA and medical therapy. METHODS: Patients diagnosed with CTEPH were included in the registry that was set up in 18 centres from August 2009 to July 2018. The characteristics and survival of patients with CTEPH receiving the different treatments were reported. Prognostic factors were evaluated by Cox regression model. RESULTS: A total of 593 patients with CTEPH were included. Eighty-one patients were treated with PEA, 61 with BPA and 451 with drugs. The estimated survival rates at 1, 3, 5 and 8 years were, respectively, 95.2%, 84.6%, 73.4% and 66.6% in all patients; 92.6%, 89.6%, 87.5% and 80.2% in surgical patients; and 95.4%, 88.3%, 71.0% and 64.1% in medically treated patients. The estimated survival rates at 1, 3, 5 and 7 years in patients treated with BPA were 96.7%, 88.1%, 70.0% and 70.0%, respectively. For all patients, PEA was an independent predictor of survival. Other independent risk factors were CHD, cardiac index, PVR, big endothelin-1, APE and 6MWD. CONCLUSION: This is the first multicentre prospective registry reporting baseline characteristics and estimated survival of patients with CTEPH in China. The long-term survival rates are similar to those of patients in the international and Spanish registries. PEA is an independent predictor of survival.

Risk prediction in medically treated chronic thromboembolic pulmonary hypertension.

BACKGROUND: At present, there is no generally accepted comprehensive prognostic risk prediction model for medically treated chronic thromboembolic pulmonary hypertension (CTEPH) patients. METHODS: Consecutive medically treated CTEPH patients were enrolled in a national multicenter prospective registry study from August 2009 to July 2018. A multivariable Cox proportional hazards model was utilized to derive the prognostic model, and a simplified risk score was created thereafter. Model performance was evaluated in terms of discrimination and calibration, and compared to the Swedish/COMPERA risk stratification method. Internal and external validation were conducted to validate the model performance. RESULTS: A total of 432 patients were enrolled. During a median follow-up time of 38.73 months (IQR: 20.79, 66.10), 94 patients (21.8%) died. The 1-, 3-, and 5-year survival estimates were 95.5%, 83.7%, and 70.9%, respectively. The final model included the following variables: the Swedish/COMPERA risk stratum (low-, intermediate- or high-risk stratum), pulmonary vascular resistance (PVR, ≤ or > 1600 dyn·s/cm5), total bilirubin (TBIL, ≤ or > 38 µmol/L) and chronic kidney disease (CKD, no or yes). Compared with the Swedish/COMPERA risk stratification method alone, both the derived model [C-index: 0.715; net reclassification improvement (NRI): 0.300; integrated discriminatory index (IDI): 0.095] and the risk score (C-index: 0.713; NRI: 0.300; IDI: 0.093) showed improved discriminatory power. The performance was validated in a validation cohort of 84 patients (C-index = 0.707 for the model and 0.721 for the risk score). CONCLUSIONS: A novel risk stratification strategy can serve as a useful tool for determining prognosis and guide management for medically treated CTEPH patients. TRIAL REGISTRATION: ClinicalTrials.gov (Identifier: NCT01417338).

Long non-coding RNA UCA1 correlates with elevated disease severity, Th17 cell proportion, inflammatory cytokines, and worse prognosis in acute ischemic stroke patients.

BACKGROUND: This study aimed to explore the association of long non-coding RNA urothelial carcinoma-associated 1 (lncRNA UCA1) expression with disease severity, inflammation, and prognosis in acute ischemic stroke (AIS) patients. METHODS: The lncRNA UCA1 expression of blood CD4+ T cells from 160 first-episode AIS patients and 160 non-AIS patients with high-stroke-risk factors (as controls) was detected by reverse transcription quantitative polymerase chain reaction. For AIS patients, interleukin (IL)-6, IL-17, and intracellular adhesion molecule-1 (ICAM1) were determined by enzyme-linked immunosorbent assay; Th17 cell ratio in CD4+ T cells was detected by flow cytometry. Their follow-up data were recorded up to 36 months, recurrence of stroke or death. The recurrence-free survival (RFS) analysis was assessed according to the follow-up data. RESULTS: LncRNA UCA1 expression was higher in AIS patients compared to controls (p < 0.001), and it was positively correlated to national institute of health stroke scale score (r = 0.436, p < 0.001), Th17 cell ratio (r = 0.398, p < 0.001), IL-6 (r = 0.204, p = 0.010), IL-17 (r = 0.326, p < 0.001), and ICAM1 (r = 0.276, p < 0.001) in AIS patients. Regarding prognosis, lncRNA UCA1 expression was elevated in 2-year recurrence/death AIS patients compared to those patients without recurrence or death within 2 years (p = 0.033), also increased in 3-year recurrence/death AIS patients compared to those patients without recurrence or death within 3 years (p = 0.008). Furthermore, high lncRNA UCA1 expression was associated with worse accumulating RFS (p = 0.017) in AIS patients. CONCLUSION: LncRNA UCA1 might sever as a candidate prognostic biomarker in AIS patients, suggesting its potency for AIS management.

A Medium-Frequency Fiber Bragg Grating Accelerometer Based on Flexible Hinges.

Mediumfrequency fiber Bragg grating (FBG) acceleration sensors are used in important applications in mechanical, aerospace and weapon equipment, and have strict requirements in terms of resonance frequency and sensitivity. A novel medium-frequency accelerometer, based on fiber Bragg grating and flexible hinges, is proposed in this paper. The differential structure doubles the sensitivity of the sensor while avoiding temperature effects. The structure model and principle for the sensor are introduced, the sensor's sensing characteristics are theoretically analyzed, and the structure parameters for the sensor are determined through numerical analysis. The sensing experiments show that the resonance frequency of the sensor is approximately 2800 Hz, the sensitivity is 21.8 pm/g in the flat frequency range of 50-1000 Hz, and the proposed sensor has a good temperature self-compensation function and lateral anti-interference capability.

"One-stop shop": safety and efficacy of combining atrial septal defect occlusion and left atrial appendage closure for patients with atrial septal defect and atrial fibrillation.

BACKGROUND: One-stop occlusion, which is defined as the combination of atrial septal defect [ASD] or patent foramen ovale [PFO] occlusion and left atrial appendage [LAA] closure, in patients with ASD/PFO and atrial fibrillation (AF) has not yet been investigated systematically. This study aimed to evaluate the safety and efficacy of one-stop occlusion in the treatment of adult patients with ASD/PFO and AF. METHODS: Inpatients with AF and ASD/PFO were recruited between August 2014 and April 2019. Preoperatively, transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were conducted to identify the ASD/PFO size and margin, presence of thrombus in the LAA, and LAA orifice width and depth at 0°, 45°, 90°, and 135°. After confirmation of the indications of LAA closure (LAAC) and ASD/PFO occlusion, the procedures were performed simultaneously under general anesthesia. Oral anticoagulants were administered for 45-60 days, followed with regular evaluation of TTE and TEE. RESULTS: Forty-nine patients (age, 65.6 ± 9.6 years) were recruited in this study, including 24 patients with ASD and 25 patients with PFO. They were treated with LAAC and ASD/PFO occlusion successfully. The mean ASD size and mean diameter of the ASD occluders were 14.2 ± 7.7 and 25.4 ± 8.5 mm, respectively. The mean PFO size was 3.5 ± 0.4 mm. The mean maximal LAA orifice width and depth were 20.5 ± 3.4 and 28.3 ± 3.6 mm, respectively. All patients were implanted with a Watchman device (diameter, 27.1 ± 2.9 mm). Postoperatively, all patients took anticoagulants orally for 45-60 days, and their mean postoperative follow-up duration was 29.0 ± 12.1 months. Postoperative TEE showed that all had normal positioning of the LAA and ASD/PFO occluders. At 45-60 days after operation, TEE showed that the LAA and ASD/PFO occluder were in the normal position; however, two patients who took warfarin and novel oral anticoagulants, respectively, have developed occluder thrombosis. After adjusted anticoagulant therapy, TEE showed that the thrombus disappeared at 6 months after operation. CONCLUSION: One-stop occlusion is safe and effective for the treatment of adult patients with ASD/PFO and AF. It is also feasible to administer warfarin or novel oral anticoagulants after operation.

MicroRNA-362-3p Targets PAX3 to Inhibit the Development of Glioma through Mediating Wnt/ß-Catenin Pathway.

BACKGROUND: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-362-3p is important in regulating the genesis of different cancers; however, the mechanism of miR-362-3p in the progression of glioma remains largely unknown. OBJECTIVES: This study aimed to elucidate pathobiological functions of miR-362-3p by targeting PAX3 in glioma. METHOD: qRT-PCR and western blotting were used to examine miR-362-3p and PAX3 expression in glioma tissues and cells. CCK-8 assay and transwell assays were used to examine the functions of miR-362-3p on human glioma. Two bioinformatics analysis software and luciferase reporter assay were performed to analyze the relationship between miR-362-3p and PAX3. RESULTS: MiR-362-3p was downregulated, and PAX3 was upregulated in glioma tissues and cells. Functional assays revealed that ectopic expression of miR-362-3p inhibited glioma cell proliferation and migration. Further, PAX3 was confirmed as direct target gene of miR-362-3p, and downregulation of PAX3 reversed the suppressive effects of miR-362-3p in glioma. In addition, miR-362-3p also exhibited suppressive effect on epithelial-mesenchymal transition and Wnt/ß-catenin pathway. CONCLUSIONS: MiR-362-3p downregulation or PAX3 overexpression predicted poor prognosis in glioma. MiR-362-3p played a role in the suppressive effect on glioma by targeting PAX3 through suppressing Wnt/ß-catenin pathway.

Safety and efficacy of ultrathin strut biodegradable polymer sirolimus-eluting stent versus durable polymer drug-eluting stents: a meta-analysis of randomized trials.

BACKGROUND: The Orsiro biodegradable polymer sirolimus-eluting stent (O-SES) is a new-generation biodegradable polymer drug-eluting stent with the thinnest strut thickness to date developed to improve the percutaneous treatment of patients with coronary artery disease. We perform a meta-analysis of randomized clinical trials (RCTs) comparing the efficacy and safety of an ultra-thin, Orsiro biodegradable polymer sirolimus-eluting stent (O-SES) compared with durable polymer drug-eluting stents (DP-DESs). METHODS: Medline, Embase, and CENTRAL databases were searched for randomized controlled trials comparing the safety and efficacy of O-SES versus DP-DES. Paired reviewers independently screened citations, assessed risk of bias of included studies, and extracted data. We used the Mantel-Haenszel method to calculate risk ratio (RR) by means of a random-effects model. RESULTS: Six RCTs with a total of 6949 patients were selected. All included trials were rated as low risk of bias. The O-SES significantly reduced the risk of myocardial infarction (RR 0.78, 95% confidence interval [CI] 0.62-0.98; I2 = 0%; 10 fewer per 1000 [from 1 fewer to 18 fewer]; high quality) compared with the DP-DES. There was no significant difference between O-SES and DP-DES in the prevention of stent thrombosis (RR: 0.75; 95% CI: 0.52-1.08), cardiac death (RR: 0.93; 95% CI: 0.63-1.36), target lesion revascularization (RR 1.10, 95% CI 0.86-1.42) and target vessel revascularization (RR 0.97, 95% CI 0.78-1.21). CONCLUSION: Among patients undergoing percutaneous coronary intervention, O-SES resulted in significantly lower rates of myocardial infarction than DP-DES and had a trend toward reduction in stent thrombosis.

RANKL Reduces Body Weight and Food Intake via the Modulation of Hypothalamic NPY/CART Expression.

The receptor activator of nuclear factor-κB ligand (RANKL) modulates energy metabolism. However, how RANKL regulates energy homeostasis is still not clear. This study aims to investigate the central mechanisms by which central administration of RANKL inhibits food intake and causes weight loss in mice. We carried out a systematic and in-depth analysis of the neuronal pathways by which RANKL mediates catabolic effects. After intracerebroventricle (i.c.v.) injection of RANKL, the expression of neuropeptide Y (NPY) mRNA in the Arc was significantly decreased, while the CART mRNA expression dramatically increased in the Arc and DMH. However, the agouti-related protein (AgRP) and pro-opiomelanocortin (POMC) mRNA had no significant changes compared with control groups. Together, the results suggest that central administration of RANKL reduces food intake and causes weight loss via modulating the hypothalamic NPY/CART pathways.

Intracoronary electrocardiogram during alcohol septal ablation for hypertrophic obstructive cardiomyopathy predicts myocardial injury size.

Alcohol septal ablation (ASA) has been used widely to treat patients with hypertrophic obstructive cardiomyopathy (HOCM). During the routine ASA procedure, it is difficult to detect the septal injury in real-time. The aim of the present study is to assess myocardial injury during ASA by recording intracoronary electrocardiogram (IC-ECG). From 2012 to 2015, 31 HOCM patients were treated with ASA, and IC-ECG was recorded in 21 patients successfully before and after ethanol injection. The elevation of ST-segment on IC-ECG after ethanol injection was expressed as its ratio to the level before injection or the absolute increasing value. Blood samples were collected before and after ASA for measuring changes in cardiac biomarkers. The ratio value of ST-segment elevation was positively correlated with both the amount of ethanol injected (r = 0.645, P = 0.001) and the myocardial injury size (creatine kinase-MB area under the curve (AUC) of CK-MB) (r = 0.466, P = 0.017). The absolute increment of ST-segment was also positively associated with both the amount of ethanol (r = 0.665, P = 0.001) and AUC of CK-MB (0.685, P = 0.001). However, there was no statistical correlation between the reduction of left ventricular outflow tract gradient and ST-segment elevation. Additionally no severe ASA procedure-related complications were observed in our patients. In conclusion, myocardial injury induced by ethanol injection can be assessed immediately by ST-segment elevation on IC-ECG. This study is the first to show that IC-ECG is a useful method for predicting myocardial injury during ASA in real-time.

Influence of Cognitive Behavioral Therapy on Mood and Quality of Life After Stent Implantation in Young and Middle-Aged Patients With Coronary Heart Disease.

Cognitive behavioral therapy (CBT), established only a few decades ago, is widely used by clinical psychologists. This study aimed to investigate the effects of CBT on mental status and quality of life (QOL) after percutaneous coronary intervention (PCI) in young and middle-aged patients with coronary heart disease (CHD). Seventy-five anxiety/depression patients (mean age, 52.2 ± 6.2 years, including 8 individuals < 45 years old) with CHD treated with PCI were randomly divided into a CBT group (n = 38) and control group (n = 37). The CBT group received 8 weeks of CBT in addition to the routine postoperative treatment that was also administered to control patients. The 17-item Hamilton Depression Rating Scale (HAM-D17), Hamilton anxiety scale (HAM-A), and Coronary Revascularization Outcome Questionnaire (CROQ-PTCA-POST, Chinese version) were administered before, 3 days, and 8 weeks after intervention. HAM-D17 and HAM-A scores were decreased after treatment, but were more substantially reduced in patients that underwent CBT than those in the control group (11.7 ± 4.5 versus 15.1 ± 3.9, P = 0.001 and 10.6 ± 3.4 versus 16.5 ± 4.6, P = 0.003, respectively). QOL was improved in both groups, but overall satisfaction was higher in the CBT group compared with control patients (89.3 ± 5.2 versus 77.8 ± 9.5, P < 0.05). CBT can relieve depression and anxiety after PCI in young and middle-aged patients with CHD. CBT can improve patient QOL.

Nifedipine inhibits ox-LDL-induced lipid accumulation in human blood-derived macrophages.

Studies have shown that nifedipine, an anti-hypertensive drug, protects against atherosclerotic progression, but the underlying mechanisms remain elusive. Oxidized low-density lipoprotein (ox-LDL) is critically implicated in macrophage lipid deposition seen in atherosclerosis. In this study, we examined the effects of nifedipine on some ox-LDL-associated changes in human blood-derived macrophages. We isolated monocytes from normal human blood and differentiated them into macrophages. We then treated these human macrophages with ox-LDL and/or nifedipine, and examined lipid accumulation and expression levels of two scavenge receptors CD36 and SR-A as well as a protein kinase PKC-θ. Nifedipine treatment substantially reduced lipid accumulation and the expression of CD36, SR-A, and protein kinase C (PKC)-θ in human macrophages treated with ox-LDL. Silencing of PKC-θ using siRNA also reduced the expression of CD36 and SR-A in these cells. Our results thus suggest that nifedipine may inhibit atherosclerosis by reducing ox-LDL-induced lipid deposition through suppression of the CD36/SR-A-mediated uptake of ox-LDL by macrophages via a PKC-θ-dependent mechanism.

Electric-Pulse Current Stimulation Increases If Current in mShox2 Genetically Modified Canine Mesenchymal Stem Cells.

OBJECTIVE: We aimed to investigate the role of mShox2 in generating If pacemaker current in vitro by means of electric-pulse current stimulation (EPCS) of canine mesenchymal stem cells (cMSCs). METHODS: mShox2 genetically modified cMSCs were prepared with pLentis-mShox2 red fluorescent protein. After EPCS induction, we examined the kinetic characteristics of generated inward current by means of a patch clamp. We then evaluated the expression of pacemaker-related genes, such as Nkx2.5, Tbx3, HCN4, Cx43 and Cx45, by means of qRT-PCR and Western blotting. The morphological changes and the cardiomyogenic differentiation marker cTnT were investigated at the same time. RESULTS: The time- and voltage-dependent inward current recorded after mShox2 infection was confirmed to be If current. After EPCS induction, the detection rate of this If current was increased. The current amplitude and density were increased, and the channel activation curve shifted to the right. The pacemaker markers Tbx3, HCN4 and Cx45 were significantly upregulated, but the working myocardium markers Nkx2.5 and Cx43 were downregulated after mShox2 infection, and were more remarkable after EPCS induction. The cells became larger and assumed spindle and spider-like morphologies. cTnT was also detected in the experimental cells. CONCLUSIONS: Our results suggest that EPCS promotes the differentiation of mShox2 genetically modified cMSCs into pacemaker-like cells, which generates more If current.